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Vasoconstriction
Kinds of Vasoconstriction Terms modified by Vasoconstriction Selected AbstractsDisparity in regional and systemic circulatory capacities: do they affect the regulation of the circulation?ACTA PHYSIOLOGICA, Issue 4 2010J. A. L. Calbet Abstract In this review we integrate ideas about regional and systemic circulatory capacities and the balance between skeletal muscle blood flow and cardiac output during heavy exercise in humans. In the first part of the review we discuss issues related to the pumping capacity of the heart and the vasodilator capacity of skeletal muscle. The issue is that skeletal muscle has a vast capacity to vasodilate during exercise [,300 mL (100 g),1 min,1], but the pumping capacity of the human heart is limited to 20,25 L min,1 in untrained subjects and ,35 L min,1 in elite endurance athletes. This means that when more than 7,10 kg of muscle is active during heavy exercise, perfusion of the contracting muscles must be limited or mean arterial pressure will fall. In the second part of the review we emphasize that there is an interplay between sympathetic vasoconstriction and metabolic vasodilation that limits blood flow to contracting muscles to maintain mean arterial pressure. Vasoconstriction in larger vessels continues while constriction in smaller vessels is blunted permitting total muscle blood flow to be limited but distributed more optimally. This interplay between sympathetic constriction and metabolic dilation during heavy whole-body exercise is likely responsible for the very high levels of oxygen extraction seen in contracting skeletal muscle. It also explains why infusing vasodilators in the contracting muscles does not increase oxygen uptake in the muscle. Finally, when ,80% of cardiac output is directed towards contracting skeletal muscle modest vasoconstriction in the active muscles can evoke marked changes in arterial pressure. [source] Vasoconstriction as the Etiology of Hypercalcemia-induced SeizuresEPILEPSIA, Issue 5 2004Tsung-Hua Chen Summary: Purpose: Reversible cerebral vasoconstriction has been hypothesized to be the etiology of seizures due to hypercalcemia, but angiographic studies documenting vasoconstriction have not previously been available. Methods: We present a 43-year-old woman who had frequent seizures that later evolved to status epilepticus with marked hypercalcemia at the time of the seizures. Results: Magnetic resonance imaging (MRI) of the patient's brain revealed high signal changes in T2 -weighted imaging, fluorescence-attenuated inversion recovery (FLAIR), and diffusion-weighted imaging (DWI) over the bilateral occipital and thalamic areas. Cerebral angiography showed blood vessels narrowing, disappearing altogether over the right posterior cerebral artery (PCA) branch, which is compatible with vasoconstriction. Vasoconstriction caused the MRI high signal in the occipital area, which was associated with subsequent periodic lateralized epileptic discharges. The patient's clinical condition improved with management of seizures and hypercalcemia. A second brain MRI 2 weeks later revealed complete resolution of the high-signal lesions. Follow-up cerebral angiography study also showed total recovery of vasoconstriction. Conclusions: The sequence of events suggests the hypothesis that reversible cerebral vasoconstriction may play a role in hypercalcemia-induced seizures. [source] Ascorbate Inhibits Reduced Arteriolar Conducted Vasoconstriction in Septic Mouse Cremaster MuscleMICROCIRCULATION, Issue 7 2007REBECCA L. MCKINNON ABSTRACT Objective: The mechanism of neuronal nitric oxide synthase (nNOS)-dependent reduction in arteriolar conducted vasoconstriction in sepsis, and the possible protection by antioxidants, are unknown. The authors hypothesized that ascorbate inhibits the conduction deficit by reducing nNOS-derived NO production. Methods: Using intravital microscopy and the cecal ligation and perforation (CLP) model of sepsis (24 h), arterioles in the cremaster muscle of male C57BL/6 wild-type mice were locally stimulated with KCl to initiate conducted vasoconstriction. The authors used the ratio of conducted constriction (500 , m upstream) to local constriction as an index of conduction (CR500). Cremaster muscle NOS enzymatic activity and protein expression, and plasma nitrite/nitrate levels were determined in control and septic mice. Intravenous ascorbate bolus (200 mg/kg in 0.1 ml of saline) was given early (0 h) or delayed at 23 h post CLP. Results: Sepsis reduced CR500 from 0.73 ± 0.03 to 0.21 ± 0.03, increased nNOS activity from 87 ± 9 to 220 ± 29 pmol/mg/h and nitrite/nitrate from 16 ± 1 to 39 ± 3 , M, without affecting nNOS protein expression. Ascorbate at 0 and 23 h prevented/reversed the conduction deficit and the increases in nNOS activity and nitrite/nitrate level. NO donor SNAP (S -nitroso- N -acetylpenicillamine) reestablished the conduction deficit in ascorbate-treated septic mice. Superoxide scavenger MnTBAP (Mn(III)tetrakis(4-benzoic acid)porphyrin chloride) did not affect this deficit. Conclusion: These data indicate that early and delayed intravenous boluses of ascorbate prevent/reverse sepsis-induced deficit in arteriolar conducted vasoconstriction in the cremaster muscle by inhibiting nNOS-derived NO production. [source] The Role of K+ Channels in Determining Pulmonary Vascular Tone, Oxygen Sensing, Cell Proliferation, and Apoptosis: Implications in Hypoxic Pulmonary Vasoconstriction and Pulmonary Arterial HypertensionMICROCIRCULATION, Issue 8 2006ROHIT MOUDGIL ABSTRACT Potassium channels are tetrameric, membrane-spanning proteins that selectively conduct K+ at near diffusion-limited rates. Their remarkable ionic selectivity results from a highly-conserved K+ recognition sequence in the pore. The classical function of K+ channels is regulation of membrane potential (EM) and thence vascular tone. In pulmonary artery smooth muscle cells (PASMC), tonic K+ egress, driven by a 145/5 mM intracellular/extracellular concentration gradient, contributes to a EM of about ,60 mV. It has been recently discovered that K+ channels also participate in vascular remodeling by regulating cell proliferation and apoptosis. PASMC express voltage-gated (Kv), inward rectifier (Kir), calcium-sensitive (KCa), and two-pore (K2P) channels. Certain K+ channels are subject to rapid redox regulation by reactive oxygen species (ROS) derived from the PASMC's oxygen-sensor (mitochondria and/or NADPH oxidase). Acute hypoxic inhibition of ROS production inhibits Kv1.5, which depolarizes EM, opens voltage-sensitive, L-type calcium channels, elevates cytosolic calcium, and initiates hypoxic pulmonary vasoconstriction (HPV). Hypoxia-inhibited K+ currents are not seen in systemic arterial SMCs. Kv expression is also transcriptionally regulated by HIF-1, and NFAT. Loss of PASMC Kv1.5 and Kv2.1 contributes to the pathogenesis of pulmonary arterial hypertension (PAH) by causing a sustained depolarization, which increases intracellular calcium and K+, thereby stimulating cell proliferation and inhibiting apoptosis, respectively. Restoring Kv expression (via Kv1.5 gene therapy, dichloroacetate, or anti-survivin therapy) reduces experimental PAH. Electrophysiological diversity exists within the pulmonary circulation. Resistance PASMC have a homogeneous Kv current (including an oxygen-sensitive component), whereas conduit PASMC current is a Kv/KCa mosaic. This reflects regional differences in expression of channel isoforms, heterotetramers, splice variants, and regulatory subunits as well as mitochondrial diversity. In conclusion, K+ channels regulate pulmonary vascular tone and remodeling and constitute potential therapeutic targets in the regression of PAH. [source] Independence of Connexin Expression and Vasomotor Conduction from Sympathetic Innervation in Hamster Feed ArteriesMICROCIRCULATION, Issue 5 2004ROBIN C. LOOFT-WILSON ABSTRACT Objective: Vasomotor responses can travel along the wall of resistance microvessels by two distinct mechanisms: cell-to-cell conduction through gap junctions or the release of neurotransmitter along perivascular nerves. It is unknown whether vascular innervation influences the expression of connexin molecules which comprise gap junctions, or the conduction of vasomotor responses. In feed arteries of the hamster retractor muscle (RFA), the authors tested whether sympathetic denervation would alter the expression of connexin isoforms and the conduction of vasomotor responses. Methods: Using intact vessels with sympathetic innervation and those 7,8 days following denervation surgery, mRNA expression was quantified using real-time PCR, cellular localization of Cx protein was characterized using immunohistochemistry, and vasomotor responses to dilator and constrictor stimuli were evaluated in isolated pressurized RFA. Results: Connexin protein localization and mRNA expression were similar between innervated and denervated vessels. mRNA levels were Cx43 = Cx37 > Cx45 , Cx40. Vasodilation to acetylcholine conducted ,2000 , m along innervated and denervated vessels, as did the biphasic conduction of vasoconstriction and vasodilation in response to KCl. Vasoconstriction to phenylephrine conducted < 500 , m and was attenuated (p < .05) in denervated vessels. Conclusions: The profile of connexin expression and the conduction of vasomotor responses are largely independent of sympathetic innervation in feed arteries of the hamster retractor muscle (RFA). [source] Left Atrial Catheter Ablation Promotes Vasoconstriction of the Right Coronary ArteryPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 2007EIJI YAMASHITA M.D. Background: Multiple cardiac ganglia are present in the left atrial (LA) region, and marked changes in autonomic nervous activity can occur after left atrial catheter ablation (CA) for atrial fibrillation (AF). Vasospastic angina involving the inferior wall of the left ventricle has been reported as a complication shortly after LACA. Methods: We studied 20 patients with drug-refractory AF who underwent LACA, performed to encircle the left- and right-sided pulmonary veins, 1 to 2 cm from their ostia under fluoroscopic guidance. Quantitative coronary angiography was performed before and after LACA, and we analyzed the minimal lesion diameter (MLD) of the proximal segment of the coronary arteries, and the basal tone, the baseline percent constriction versus maximal dilation after nitroglycerin administration. Results: No significant difference was observed in MLD or basal tone of the left coronary arteries after LACA. However, in the right coronary artery (RCA), the basal MLD was smaller (P < 0.01) and the basal tone was greater (P< 0.05) after than before LACA. No correlation was found between the baseline MLD or tone of the RCA and total amount of radiofrequency energy delivered or procedure duration. In 75% of RCA, the baseline MLD was smaller after than before LACA, which was significantly higher (P < 0.01) than observed in the left coronary arteries (38%). Conclusion: Vasoconstriction was promoted in the RCA shortly after LACA, which may explain the variant angina reported after LACA. [source] Vibration Causes Acute Vascular Injury in a Two-Step Process: Vasoconstriction and Vacuole DisruptionTHE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 8 2008Sandya R. Govindaraju Abstract Hand,arm vibration syndrome is a vasospastic and neurodegenerative occupational disease. In the current study, the mechanism of vibration-induced vascular smooth muscle cell (SMC) injury was examined in a rat-tail vibration model. Tails of male Sprague Dawley rats were vibrated continuously for 4 hr at 60 Hz, 49 m/s2 with or without general anesthesia. Ventral tail arteries were aldehyde fixed and embedded in epoxy resin to enable morphological analysis. Vibration without anesthesia caused vasoconstriction and vacuoles in the SMC. Anesthetizing rats during vibration prevented vasoconstriction and vacuole formation. Exposing tail arteries in situ to 1 mM norepinephrine (NE) for 15 min induced the greatest vasoconstriction and vacuolation. NE induced vacuoles were twice as large as those formed during vibration. When vibrated 4 hr under anesthesia after pretreatment with NE for 15 min, the SMC lacked vacuoles and exhibited a longitudinal banding pattern of dark and light staining. The extracellular matrix was filled with particulates, which were confirmed by electron microscopy to be cellular debris. The present findings demonstrate that vibration-induced vasoconstriction (SMC contraction) requires functioning central nervous system reflexes, and the physical stress of vibration damages the contracted SMC by dislodging and fragmenting SMC vacuoles. Anat Rec, 291:999,1006, 2008. © 2008 Wiley-Liss, Inc. [source] Vasoconstrictively Acting AT1R A1166C and NOS3 4/5 Polymorphisms in Recurrent Spontaneous Abortions (RSA),AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 5 2004Tina Buchholz Problem:, Inadequate uteroplacental perfusion is one of the main reasons for recurrent spontaneous abortions (RSA). Coagulation, fibrinolysis, and vasoconstriction affect tissue perfusion. These systems are regulated by different gene products. Polymorphisms can modulate the expression levels of the respective genes and can thereby affect perfusion. Vasoconstriction is influenced by the expression of endothelial nitric oxide synthase (eNOS) and of the angiotensinogen II type 1 receptor (AT1R). Method:, The aim of our study was to investigate, whether two polymorphisms in the AT1R and NOS3 genes shown to result in maternal vasoconstriction are associated with an increased risk for RSA. Results:, Our data indicate that the vasoconstrictively acting genotypes AT1R C/C and NOS3 4/4 are of similar prevalence in RSA patients and in controls. Conclusion:, Results do not show any influence of the polymorphisms studied on early pregnancy development. This is in concordance with the concept of an independent regulation of placental perfusion. [source] Magnetic resonance angiography in reversible cerebral vasoconstriction syndromesANNALS OF NEUROLOGY, Issue 5 2010Shih-Pin Chen MD Objective To investigate the evolution and clinical significance of vasoconstriction on magnetic resonance angiography (MRA) in patients with reversible cerebral vasoconstriction syndromes (RCVS). Methods Patients with RCVS were recruited and followed up with MRA examinations until normalization of vasoconstriction or for 6 months. The vasoconstriction severity of the major cerebral arterial segments (M1, M2, A1, A2, P1, P2, and basilar artery) was scored on a 5-point scale: 0 (0,<10%), 1 (10,<25%), 2 (25,<50%), 3 (50,<75%), and 4 (,75%). Subjects with at least 1 segment with a vasoconstriction score ,2 were eligible for the study. Initial mean scores of single or combined arterial segments were used to predict ischemic complications. Results Seventy-seven patients with RCVS (8 men/69 women; average age 47.7 ± 11.6 years) finished the study with a total of 225 MRAs performed. The mean number of arterial segments involved was 5.3 ± 3.0 in the initial MRA. Vasoconstriction scores reached their maximum 16.3 ± 10.2 days after headache onset, close to the average timing of headache resolution (16.7 ± 8.6 days). Vasoconstriction evolved in a parallel trend among different arterial segments. Seven (9.1%) patients developed posterior reversible encephalopathy syndromes (PRES). Six (7.8%) patients had ischemic stroke. A logistic regression model demonstrated that the M1,P2 combined score was associated with highest risk of PRES (odds ratio [OR], 11.6, p = 0.005) and ischemic stroke (OR, 3.4; p = 0.026). Interpretation MRA evaluation in patients with RCVS is valid. Vasoconstriction was pervasive and outlasted headache resolution. Vasoconstrictions in M1 and P2 are important determinants for PRES and ischemic stroke. ANN NEUROL 2010;67:648,656 [source] Vasopressin-induced facilitation of adrenergic responses in the rat mesenteric artery is V1 -receptor dependentAUTONOMIC & AUTACOID PHARMACOLOGY, Issue 1 2003J. O. Streefkerk Summary 1 The present study was designed to analyse the possible involvement of V1 - and V2 -receptors in vasopressin (AVP)-induced facilitation of the sympathetic nervous system. Furthermore, we aimed to determine whether the site of facilitation by AVP is located pre- or postsynaptically. 2 Electrical field stimulation (EFS) was applied on the rat mesteric artery to activate the sympathetic nervous system. In addition, we evaluated the direct vascular effects of AVP. The postsynaptic effect of AVP on the sympathetic nervous system was investigated by exposing the vessels to exogenous noradrenaline. These experiments were performed in the absence or presence of selective V1 and V2 receptor antagonists SR 49059 and SR 121463, respectively. Desmopressin was applied as a selective V2 agonist. 3 The direct vasoconstrictor effect of AVP was antagonized by SR 49059 and not by SR 121463. Desmopressin neither showed any direct vasoconstrictor effect nor produced vasodilatation after a precontraction induced by noradrenaline (10 ,m). The EFS-induced rise in vascular tone could be increased by a sub-pressor concentration of AVP. This fascilitation could be antagonized by SR 49059, but not by SR 121463. Desmopressin did not influence the increase in vascular tone during EFS. Vasoconstriction induced by exogenous noradrenaline could be facilitated by a sub-pressor concentration of AVP and this selective postsynaptic effect could be antagonized by V1 -receptor blockade. 4 In conclusion, the AVP-induced facilitation of the sympathetic nervous system is completely V1 -receptor dependent and at least partly postsynaptically mediated. [source] Pharmacodynamics and dermatopharmacokinetics of betamethasone 17-valerate: assessment of topical bioavailabilityBRITISH JOURNAL OF DERMATOLOGY, Issue 3 2009S. Wiedersberg Summary Background, The bioavailability of most topically delivered drugs is difficult to quantify, but is generally believed to be very low. With the exception of the vasoconstrictor assay for corticosteroids, no methodology to quantify the rate and extent of drug delivery to the skin has been validated. Recent research has examined the dermatopharmacokinetic (DPK) technique, which is based on stratum corneum (SC) tape-stripping. Objective, To compare the in vivo bioavailability of different topical formulations of betamethasone 17-valerate (BMV) using the vasoconstrictor assay and the DPK method. Methods, BMV was formulated in different vehicles and the drug concentration was adjusted to either (i) equal thermodynamic activity, or (ii) a range of values up to that corresponding to 80% of maximum thermodynamic activity. Vasoconstriction, an accepted and widely used method to determine bioavailability and bioequivalence of topical steroids, was quantified with a chromameter over 24 h post-removal of the formulation. Drug uptake into the SC was assessed by tape-stripping. Results, BMV at the same thermodynamic activity in different vehicles provoked similar skin blanching responses, while DPK profiles distinguished between the formulations. Further, skin blanching responses and drug uptake into the SC clearly depended upon the absolute BMV concentration applied. However, while the saturable nature of the pharmacodynamic response was clear, the tape-stripping method distinguished unequivocally between the different formulations and different concentrations. Conclusions, The DPK approach offers a reliable metric with which to quantify transfer of drug from the vehicle to the SC, and may be useful for topical bioavailability and bioequivalence determinations. [source] The therapeutic effects of retinal laser treatment and vitrectomy.ACTA OPHTHALMOLOGICA, Issue 5 2001A theory based on oxygen, vascular physiology ABSTRACT. The physiologic mechanism of photocoagulation can been seen in the following steps. The physical light energy is absorbed in the melanin of the retinal pigment epithelium. The adjacent photoreceptors are destroyed and are replaced by a glial scar and the oxygen consumption of the outer retina is reduced. Oxygen that normally diffuses from the choriocapillaris into the retina can now diffuse through the laser scars in the photoreceptor layer without being consumed in the mitochondria of the photoreceptors. This oxygen flux reaches the inner retina to relieve inner retinal hypoxia and raise the oxygen tension. As a result, the retinal arteries constrict and the bloodflow decreases. Hypoxia relief reduces production of growth factors such as VEGF and neovascularization is reduced or stopped. Vasoconstriction increases arteriolar resistance, decreases hydrostatic pressure in capillaries and venules and reduces edema formation according to Starling's law. Vitrectomy also improves retinal oxygenation by allowing oxygen and other nutrients to be transported in water currents in the vitreous cavity from well oxygenated to ischemic areas of the retina. Vitrectomy and retinal photocoagulation both improve retinal oxygenation and both reduce diabetic macular edema and retinal neovascularization. [source] Magnetic resonance angiography in reversible cerebral vasoconstriction syndromesANNALS OF NEUROLOGY, Issue 5 2010Shih-Pin Chen MD Objective To investigate the evolution and clinical significance of vasoconstriction on magnetic resonance angiography (MRA) in patients with reversible cerebral vasoconstriction syndromes (RCVS). Methods Patients with RCVS were recruited and followed up with MRA examinations until normalization of vasoconstriction or for 6 months. The vasoconstriction severity of the major cerebral arterial segments (M1, M2, A1, A2, P1, P2, and basilar artery) was scored on a 5-point scale: 0 (0,<10%), 1 (10,<25%), 2 (25,<50%), 3 (50,<75%), and 4 (,75%). Subjects with at least 1 segment with a vasoconstriction score ,2 were eligible for the study. Initial mean scores of single or combined arterial segments were used to predict ischemic complications. Results Seventy-seven patients with RCVS (8 men/69 women; average age 47.7 ± 11.6 years) finished the study with a total of 225 MRAs performed. The mean number of arterial segments involved was 5.3 ± 3.0 in the initial MRA. Vasoconstriction scores reached their maximum 16.3 ± 10.2 days after headache onset, close to the average timing of headache resolution (16.7 ± 8.6 days). Vasoconstriction evolved in a parallel trend among different arterial segments. Seven (9.1%) patients developed posterior reversible encephalopathy syndromes (PRES). Six (7.8%) patients had ischemic stroke. A logistic regression model demonstrated that the M1,P2 combined score was associated with highest risk of PRES (odds ratio [OR], 11.6, p = 0.005) and ischemic stroke (OR, 3.4; p = 0.026). Interpretation MRA evaluation in patients with RCVS is valid. Vasoconstriction was pervasive and outlasted headache resolution. Vasoconstrictions in M1 and P2 are important determinants for PRES and ischemic stroke. ANN NEUROL 2010;67:648,656 [source] Chronic lung disease: oxygen dogma revisitedACTA PAEDIATRICA, Issue 2 2001O D Saugstad Since the discovery of retrolental fibroplasia, and the role of oxygen in its development, oxygen has been considered a double-edged sword in neonatal medicine, the utmost care being exercised in order not to give too much oxygen (1). However, the important observation that hypoxaemia might induce pulmonary vasoconstriction (2) and airway constriction (3) in infants at risk for bronchopulmonary dysplasia has resulted in only a minor upward adjustment of oxygen supplementation in many neonatal units. Since oxygen toxicity has long been linked not only to retinopathy of prematurity but also to bronchopulmonary dysplasia (4), it is relevant to ask whether an increased FiO2 might have any detrimental effects on babies. [source] Uridine adenosine tetraphosphate affects contractility of mouse aorta and decreases blood pressure in conscious rats and miceACTA PHYSIOLOGICA, Issue 2 2010P. B. Hansen Abstract Aim:, In the anaesthetized rat, uridine adenosine tetraphosphate (Up4A) is a circulating, endothelium-derived vasoconstrictor presumably operating as such in un-anaesthetized animals. The present study investigated the in vivo effects of Up4A in conscious mice and rats, and its direct vascular effects in the mouse aorta in vitro. Methods:,In vivo, Up4A was given as step-up infusion at rates of 8,512 nmol min,1 kg,1 for 30 min periods in chronically catheterized rodents. In vitro, the effect of Up4A on rings of mouse aortae mounted in a myograph was tested. Results:, High doses of Up4A (mice: 512 nmol min,1 kg,1; rats: 128 nmol min,1 kg,1) caused hypotension (99 ± 4 to 64 ± 7 mmHg and 114 ± 3 to 108 ± 3 mmHg, respectively, both P < 0.01). In rats, Up4A significantly decreased sodium excretion by >75% and potassium excretion by ,60% without significant changes in urine flow. Exposure of phenylephrine-contracted rings to increasing concentrations of Up4A elicited contraction at 10,7 and 10,6 mol L,1 (18 ± 2% and 76 ± 16% respectively); unexpectedly, 10,5 mol L,1 caused a biphasic response with a contraction (19 ± 6%) followed by a relaxation (,46 ± 6%). No relaxation was observed when the concentration was increased further. Bolus exposure to 10,5 mol L,1 of Up4A caused contraction (+80 ± 2%). Added successively to untreated vessels, increasing concentrations of Up4A (10,7,10,5 mol L,1) induced a biphasic response of contraction followed by relaxation. Conclusion:, Up4A has direct biphasic effects on vascular smooth muscle of the mouse aorta but vasoconstriction dominates at low concentrations. In conscious rodents, step-up infusions of Up4A elicit hypotension and electrolyte retention. [source] Tubular reabsorption and diabetes-induced glomerular hyperfiltrationACTA PHYSIOLOGICA, Issue 1 2010P. Persson Abstract Elevated glomerular filtration rate (GFR) is a common observation in early diabetes mellitus and closely correlates with the progression of diabetic nephropathy. Hyperfiltration has been explained to be the result of a reduced load of sodium and chloride passing macula densa, secondarily to an increased proximal reabsorption of glucose and sodium by the sodium-glucose co-transporters. This results in an inactivation of the tubuloglomerular feedback (TGF), leading to a reduced afferent arteriolar vasoconstriction and subsequently an increase in GFR. This hypothesis has recently been questioned due to the observation that adenosine A1 -receptor knockout mice, previously shown to lack a functional TGF mechanism, still display a pronounced hyperfiltration when diabetes is induced. Leyssac demonstrated in the 1960s (Acta Physiol Scand58, 1963:236) that GFR and proximal reabsorption can work independently of each other. Furthermore, by the use of micropuncture technique a reduced hydrostatic pressure in Bowman's space or in the proximal tubule of diabetic rats has been observed. A reduced pressure in Bowman's space will increase the pressure gradient over the filtration barrier and can contribute to the development of diabetic hyperfiltration. When inhibiting proximal reabsorption with a carbonic anhydrase inhibitor, GFR decreases and proximal tubular pressure increases. Measuring intratubular pressure allows a sufficient time resolution to reveal that net filtration pressure decreases before TGF is activated which highlights the importance of intratubular pressure as a regulator of GFR. Taken together, these results imply that the reduced intratubular pressure observed in diabetes might be crucial for the development of glomerular hyperfiltration. [source] Muscle metaboreflex control of the circulation during exerciseACTA PHYSIOLOGICA, Issue 4 2010R. Boushel Abstract This review covers the control of blood pressure, cardiac output and muscle blood flow by the muscle metaboreflex which involves chemically sensitive nerves located in muscle parenchyma activated by metabolites accumulating in the muscle during contraction. The efferent response to metaboreflex activation is an increase in sympathetic nerve activity that constricts the systemic vasculature and also evokes parallel inotropic and chronotropic effects on the heart to increase cardiac output. The metaboreflex elicits a significant blood pressure elevating response during exercise and functions to redistribute blood flow and blood volume. Regional specificity in the efferent response to the metaboreflex activated from either the leg or the arm is seen in the balance between signals for vasoconstriction to curtail blood flow and signals to increase cardiac output. The metaboreflex has dual functions. It can both elevate and decrease muscle blood flow depending on (1) the intensity and mode of contraction, (2) the limb in which the reflex is evoked, (3) the strength of the signal defined by the muscle mass, (4) the extent to which blood flow is redistributed from inactive vascular beds to increase central blood volume and (5) the extent to which cardiac output can be increased. [source] Disparity in regional and systemic circulatory capacities: do they affect the regulation of the circulation?ACTA PHYSIOLOGICA, Issue 4 2010J. A. L. Calbet Abstract In this review we integrate ideas about regional and systemic circulatory capacities and the balance between skeletal muscle blood flow and cardiac output during heavy exercise in humans. In the first part of the review we discuss issues related to the pumping capacity of the heart and the vasodilator capacity of skeletal muscle. The issue is that skeletal muscle has a vast capacity to vasodilate during exercise [,300 mL (100 g),1 min,1], but the pumping capacity of the human heart is limited to 20,25 L min,1 in untrained subjects and ,35 L min,1 in elite endurance athletes. This means that when more than 7,10 kg of muscle is active during heavy exercise, perfusion of the contracting muscles must be limited or mean arterial pressure will fall. In the second part of the review we emphasize that there is an interplay between sympathetic vasoconstriction and metabolic vasodilation that limits blood flow to contracting muscles to maintain mean arterial pressure. Vasoconstriction in larger vessels continues while constriction in smaller vessels is blunted permitting total muscle blood flow to be limited but distributed more optimally. This interplay between sympathetic constriction and metabolic dilation during heavy whole-body exercise is likely responsible for the very high levels of oxygen extraction seen in contracting skeletal muscle. It also explains why infusing vasodilators in the contracting muscles does not increase oxygen uptake in the muscle. Finally, when ,80% of cardiac output is directed towards contracting skeletal muscle modest vasoconstriction in the active muscles can evoke marked changes in arterial pressure. [source] Circulatory effects of apnoea in elite breath-hold diversACTA PHYSIOLOGICA, Issue 1 2009F. Joulia Abstract Aim:, Voluntary apnoea induces several physiological adaptations, including bradycardia, arterial hypertension and redistribution of regional blood flows. Elite breath-hold divers (BHDs) are able to maintain very long apnoea, inducing severe hypoxaemia without brain injury or black-out. It has thus been hypothesized that they develop protection mechanisms against hypoxia, as well as a decrease in overall oxygen uptake. Methods:, To test this hypothesis, the apnoea response was studied in BHDs and non-divers (NDs) during static and dynamic apnoeas (SA, DA). Heart rate, arterial oxygen saturation (SaO2), and popliteal artery blood flow were recorded to investigate the oxygen-conserving effect of apnoea response, and the internal carotid artery blood flow was used to examine the mechanisms of cerebral protection. Results:, The bradycardia and peripheral vasoconstriction were accentuated in BHDs compared with NDs (P < 0.01), in association with a smaller SaO2 decrease (,2.7% vs. ,4.9% during SA, P < 0.01 and ,6% vs. ,11.3% during DA, P < 0.01). Greater increase in carotid artery blood flow was also measured during apnoea in BHDs than in controls. Conclusion:, These results confirm that elite divers present a potentiation of the well-known apnoea response in both SA and DA conditions. This response is associated with higher brain perfusion which may partly explain the high levels of world apnoea records. [source] The role of the ,-adrenergic receptor in the leg vasoconstrictor response to orthostatic stressACTA PHYSIOLOGICA, Issue 3 2009M. Kooijman Abstract Aim:, The prompt increase in peripheral vascular resistance, mediated by sympathetic ,-adrenergic stimulation, is believed to be the key event in blood pressure control during postural stress. However, despite the absence of central sympathetic control of the leg vasculature, postural leg vasoconstriction is preserved in spinal cord-injured individuals (SCI). This study aimed at assessing the contribution of both central and local sympathetically induced ,-adrenergic leg vasoconstriction to head-up tilt (HUT) by including healthy individuals and SCI, who lack central sympathetic baroreflex control over the leg vascular bed. Methods:, In 10 controls and nine SCI the femoral artery was cannulated for drug infusion. Upper leg blood flow (LBF) was measured bilaterally using venous occlusion strain gauge plethysmography before and during 30° HUT throughout intra-arterial infusion of saline or the non-selective ,-adrenergic receptor antagonist phentolamine respectively. Additionally, in six controls the leg vascular response to the cold pressor test was assessed during continued infusion of phentolamine, in order to confirm complete ,-adrenergic blockade by phentolamine. Results:, During infusion of phentolamine HUT still caused vasoconstriction in both groups: leg vascular resistance (mean arterial pressure/LBF) increased by 10 ± 2 AU (compared with 12 ± 2 AU during saline infusion), and 13 ± 3 AU (compared with 7 ± 3 AU during saline infusion) in controls and SCI respectively. Conclusion:, Effective ,-adrenergic blockade did not reduce HUT-induced vasoconstriction, regardless of intact baroreflex control of the leg vasculature. Apparently, redundant mechanisms compensate for the absence of sympathetic ,-adrenoceptor leg vasoconstriction in response to postural stress. [source] Acute exercise causes an enhancement of tissue renin,angiotensin system in the kidney in ratsACTA PHYSIOLOGICA, Issue 1 2005S. Maeda Abstract Aims:, Initially, the renin,angiotensin system (RAS) produced through the classical endocrine pathway was well known for its regulation of blood pressure. However, it was revealed that a local autocrine and/or paracrine RAS may exist in a number of tissues (such as kidney). Exercise causes a redistribution of tissue blood flow, by which the blood flow is greatly increased in active muscles, whereas it is decreased in the splanchnic circulation (such as in the kidney). We hypothesized that exercise causes an enhancement of tissue RAS in the kidney. Methods:, We studied whether exercise affects expression of angiotensinogen and angiotensin-converting enzyme (ACE) and tissue angiotensin II level in the kidney. The rats performed treadmill running for 30-min. Immediately after this exercise, kidney was quickly removed. Control rats remained at rest during this 30-min period. Results:, The expression of angiotensinogen mRNA in the kidney was markedly higher in the exercise rats than in the control rats. ACE mRNA in the kidney was significantly higher in the exercise rats than in the control rats. Western blot analysis confirmed significant upregulation of ACE protein in the kidney after exercise. Tissue angiotensin II level was also increased by exercise. Conclusion:, The present study suggests that the exercise-induced enhancement of tissue RAS in the kidney causes vasoconstriction and hence decreases blood flow in the kidney, which are helpful in increasing blood flow in active muscles, thereby contributing to the redistribution of blood flow during exercise. [source] Pressure-independent cardiac effects of angiotensin II in pigsACTA PHYSIOLOGICA, Issue 2 2004M. Broomé Abstract Background:, Angiotensin II (Ang II) is a potent vasoconstrictor with an important role in the development of cardiovascular disease. Earlier results have shown a positive acute inotropic effect of Ang II in anaesthetized pigs together with significant vasoconstriction. This investigation was designed to study cardiac effects of Ang II, when blood pressure was maintained constant by experimental means. Methods:, Ang II (200 ,g h,1) was infused in anaesthetized pigs (n = 10) at two different arterial blood pressures, the first determined by the effects of Ang II alone, and the second maintained at baseline blood pressure with nitroprusside. Cardiac systolic and diastolic function was evaluated by analysis of left ventricular pressure,volume relationships. Results:, Heart rate, end-systolic elastance (Ees) and pre-load adjusted maximal power (PWRmax EDV,2) increased at both blood pressure levels, although less when blood pressure was kept constant with nitroprusside. The time constant for isovolumetric relaxation (,1/2) was prolonged with Ang II alone and shortened with Ang II infused together with nitroprusside. Conclusion:, Ang II infusion in the pig has inotropic and chronotropic properties independent of arterial blood pressure levels, although the effects seem to be blunted by pharmacological actions of the nitric oxide donor nitroprusside. [source] Calcium handling in afferent arteriolesACTA PHYSIOLOGICA, Issue 4 2004M. Salomonsson Abstract The cytosolic intracellular calcium concentration ([Ca2+]i) is a major determining factor in the vascular smooth muscle tone. In the afferent arteriole it has been shown that agonists utilizing G-protein coupled receptors recruit Ca2+ via release from intracellular stores and entry via pathways in the plasma membrane. The relative importances of entry vs. mobilization seem to differ between different agonists, species and preparations. The entry pathway might include different types of voltage sensitive Ca2+ channels located in the plasmalemma such as dihydropyridine sensitive L-type channels, T-type channels and P/Q channels. A role for non-voltage sensitive entry pathways has also been suggested. The importance of voltage sensitive Ca2+ channels in the control of the tone of the afferent arteriole (and thus in the control of renal function and whole body control of extracellular fluid volume and blood pressure) sheds light on the control of the membrane potential of afferent arteriolar smooth muscle cells. Thus, K+ and Cl, channels are of importance in their role as major determinants of membrane potential. Some studies suggest a role for calcium-activated chloride (ClCa) channels in the renal vasoconstriction elicited by agonists. Other investigators have found evidence for several types of K+ channels in the regulation of the afferent arteriolar tone. The available literature in this field regarding afferent arterioles is, however, relatively sparse and not conclusive. This review is an attempt to summarize the results obtained by others and ourselves in the field of agonist induced afferent arteriolar Ca2+ recruitment, with special emphasis on the control of voltage sensitive Ca2+ entry. Outline of the Manuscript: This manuscript is structured as follows: it begins with an introduction where the general role for [Ca2+]i as a key factor in the regulation of the tone of vascular smooth muscles (VSMC) is detailed. In this section there is an emphasis is on observations that could be attributed to afferent arteriolar function. We then investigate the literature and describe our results regarding the relative roles for Ca2+ entry and intracellular release in afferent arterioles in response to vasoactive agents, with the focus on noradrenalin (NA) and angiotensin II (Ang II). Finally, we examine the role of ion channels (i.e. K+ and Cl, channels) for the membrane potential, and thus activation of voltage sensitive Ca2+ channels. [source] No effect of venoconstrictive thigh cuffs on orthostatic hypotension induced by head-down bed restACTA PHYSIOLOGICA, Issue 2 2000M.-A. Custaud Orthostatic intolerance (OI) is the most serious symptom of cardiovascular deconditioning induced by head-down bed rest or weightlessness. Wearing venoconstrictive thigh cuffs is an empirical countermeasure used by Russian cosmonauts to limit the shift of fluid from the lower part of the body to the cardio-cephalic region. Our aim was to determine whether or not thigh cuffs help to prevent orthostatic hypotension induced by head-down bed rest. We studied the effect of thigh cuffs on eight healthy men. The cuffs were worn during the day for 7 days of head-down bed rest. We measured: orthostatic tolerance (stand tests and lower body negative pressure tests), plasma volume (Evans blue dilution), autonomic influences (plasma noradrenaline) and baroreflex sensitivity (spontaneous baroreflex slope). Thigh cuffs limited the loss of plasma volume (thigh cuffs: ,201 ± 37 mL vs. control: ,345 ± 42 mL, P < 0.05), the degree of tachycardia and reduction in the spontaneous baroreflex sensitivity induced by head-down bed rest. However, the impact of thigh cuffs was not sufficient to prevent OI (thigh cuffs: 7.0 min of standing time vs. control: 7.1 min). Decrease in absolute plasma volume and in baroreflex sensitivity are known to be important factors in the aetiology of OI induced by head-down bed rest. However, dealing with these factors, using thigh cuffs for example, is not sufficient to prevent OI. Other factors such as venous compliance, microcirculatory changes, peripheral arterial vasoconstriction and vestibular afferents must also be considered. [source] Insulin resistance and endothelial dysfunction: the road map to cardiovascular diseasesDIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 6 2006Eugenio Cersosimo Abstract Cardiovascular disease affects approximately 60% of the adult population over the age of 65 and represents the number one cause of death in the United States. Coronary atherosclerosis is responsible for the vast majority of the cardiovascular events, and a number of cardiovascular risk factors have been identified. In recent years, it has become clear that insulin resistance and endothelial dysfunction play a central role in the pathogenesis of atherosclerosis. Much evidence supports the presence of insulin resistance as the fundamental pathophysiologic disturbance responsible for the cluster of metabolic and cardiovascular disorders, known collectively as the metabolic syndrome. Endothelial dysfunction is an important component of the metabolic or insulin resistance syndrome and this is demonstrated by inadequate vasodilation and/or paradoxical vasoconstriction in coronary and peripheral arteries in response to stimuli that release nitric oxide (NO). Deficiency of endothelial-derived NO is believed to be the primary defect that links insulin resistance and endothelial dysfunction. NO deficiency results from decreased synthesis and/or release, in combination with exaggerated consumption in tissues by high levels of reactive oxygen (ROS) and nitrogen (RNS) species, which are produced by cellular disturbances in glucose and lipid metabolism. Endothelial dysfunction contributes to impaired insulin action, by altering the transcapillary passage of insulin to target tissues. Reduced expansion of the capillary network, with attenuation of microcirculatory blood flow to metabolically active tissues, contributes to the impairment of insulin-stimulated glucose and lipid metabolism. This establishes a reverberating negative feedback cycle in which progressive endothelial dysfunction and disturbances in glucose and lipid metabolism develop secondary to the insulin resistance. Vascular damage, which results from lipid deposition and oxidative stress to the vessel wall, triggers an inflammatory reaction, and the release of chemoattractants and cytokines worsens the insulin resistance and endothelial dysfunction. From the clinical standpoint, much experimental evidence supports the concept that therapies that improve insulin resistance and endothelial dysfunction reduce cardiovascular morbidity and mortality. Moreover, interventional strategies that reduce insulin resistance ameliorate endothelial dysfunction, while interventions that improve tissue sensitivity to insulin enhance vascular endothelial function. There is general agreement that aggressive therapy aimed simultaneously at improving insulin-mediated glucose/lipid metabolism and endothelial dysfunction represents an important strategy in preventing/delaying the appearance of atherosclerosis. Interventions that 1 correct carbohydrate and lipid metabolism, 2 improve insulin resistance, 3 reduce blood pressure and restore vascular reactivity, and 4 attenuate procoagulant and inflammatory responses in adults with a high risk of developing cardiovascular disease reduce cardiovascular morbidity and mortality. Whether these benefits hold when the same prevention strategies are applied to younger, high-risk individuals remains to be determined. Copyright © 2006 John Wiley & Sons, Ltd. [source] 2,2,-Nitrophenylisatogen potentiates P2X1 receptor mediated vascular contraction and blood pressure elevationDRUG DEVELOPMENT RESEARCH, Issue 1 2003Anna-Karin Wihlborg Abstract The objective of this research was to examine the effects of chemical compounds with possible P2 receptor modulating effects and to characterize the potentiating effects of 2,2,-nitrophenylisatogen (NPI) on P2X1 receptors in vitro and in vivo. Chemical compounds were tested in an in vitro pharmacological assay using vascular segments from the rat mesenteric artery stimulated by P2 receptor-specific agonists. Contractions were expressed as a percentage of 60 mM K+ -induced contractions. Blood pressure was evaluated in pithed rats. NPI (30 ,M) added 15 min before addition of the P2X1 receptor-specific agonist ,,-MeATP increased the maximum vasoconstriction from 23% to 49% (an increase of 113%). Furthermore, NPI prevented the desensitization of repeated ,,-MeATP contractions. Related compounds were examined, and 2-(3-methoxy-phenyl)-1-oxy-indol-3-one (MPI) had similar effects as NPI, but several others lacked effect. NPI had no effect on ADP,S (P2Y1) or acetylcholine-mediated vasodilatation, nor on UTP (P2Y2/4), UDP (P2Y6), or noradrenaline-mediated contractions. In pithed rats, the blood pressure response to 50 nmol/kg-infusion of ,,-MeATP was increased from 50±6 to 63±5 mmHg (P<0.05), but had no effect on basal blood pressure or on the cardiovascular response to preganglionic nerve stimulation. In conclusion, NPI and MPI potentiates P2X1 receptor vascular contractions in vitro and (NPI) blood pressure effects in vivo. It is possible that the effect is mediated by an inhibition of P2X1 receptor desensitization. Drug Dev. Res. 59:82,87, 2003. © 2003 Wiley-Liss, Inc. [source] Peroxynitrite/Nitric Oxide Balance in Ischemia/Reperfusion Injury-Nanomedical ApproachELECTROANALYSIS, Issue 4 2006Ruslan Kubant Abstract Electrochemical nanosensors were used to simultaneously monitor in vitro (a single endothelial cell) and in vivo (vasculature of rat) the concentrations of NO (vasorelaxant), cytotoxic O (oxidative stress) and ONOO, (nitroxidative stress). A balance of [NO]/[ONOO,]=(K) was applied as the diagnostic marker of dysfunctional endothelium and cardiovascular disease. In the isolated endothelium of normotensive rats, K=,2.8±0.1 while in hypertensive rats, K=0.4±0.1. During ischemia, K dropped from 7±1 to 1.4±0.2 and further decreased to 0.05±0.01 during reperfusion. The edema and vasoconstriction, indicators of vascular injury, correlated directly with the decrease in K. [source] Circulation in normal and inflamed dental pulpENDODONTIC TOPICS, Issue 1 2007ELLEN BERGGREEN In the pulp, arteries branch into a capillary network before they leave the pulp as venules through the apical foramina. The tissue has low compliance, as it is enclosed in dentin, and has a relatively high blood flow and blood volume. The interstitial fluid pressure (IFP) and colloid osmotic pressure are relatively high whereas the net driving blood pressure is low. The high pulsatile IFP is probably the major force for propelling lymph in the dental pulp. Vasodilation in neighboring tissue as well as arteriovenous (AV) shunts in the pulp itself can contribute to a fall in total and coronal pulpal blood flow, respectively. The pulp blood flow is under nervous, humoral, and local control. Inflammatory vascular responses, vasodilation, and increased vessel permeability induce an increase in IFP that can be followed by a temporarily impaired blood flow response. Lipopolysaccharides (LPS) from bacteria may cause endothelial activation in the pulp, leading to vasoconstriction and reduced vascular perfusion. Lymphatic vessels are identified with specific lymphatic markers in the pulp but so far, little is known about their function. Because of the special circulatory conditions in the pulp, there are several clinical implications that need to be considered in dental treatment. Received 13 February 2009; accepted 28 August 2009. [source] Vasoconstriction as the Etiology of Hypercalcemia-induced SeizuresEPILEPSIA, Issue 5 2004Tsung-Hua Chen Summary: Purpose: Reversible cerebral vasoconstriction has been hypothesized to be the etiology of seizures due to hypercalcemia, but angiographic studies documenting vasoconstriction have not previously been available. Methods: We present a 43-year-old woman who had frequent seizures that later evolved to status epilepticus with marked hypercalcemia at the time of the seizures. Results: Magnetic resonance imaging (MRI) of the patient's brain revealed high signal changes in T2 -weighted imaging, fluorescence-attenuated inversion recovery (FLAIR), and diffusion-weighted imaging (DWI) over the bilateral occipital and thalamic areas. Cerebral angiography showed blood vessels narrowing, disappearing altogether over the right posterior cerebral artery (PCA) branch, which is compatible with vasoconstriction. Vasoconstriction caused the MRI high signal in the occipital area, which was associated with subsequent periodic lateralized epileptic discharges. The patient's clinical condition improved with management of seizures and hypercalcemia. A second brain MRI 2 weeks later revealed complete resolution of the high-signal lesions. Follow-up cerebral angiography study also showed total recovery of vasoconstriction. Conclusions: The sequence of events suggests the hypothesis that reversible cerebral vasoconstriction may play a role in hypercalcemia-induced seizures. [source] Equine laminitis: cryotherapy reduces the severity of the acute lesionEQUINE VETERINARY JOURNAL, Issue 3 2004A. W. Van Eps Summary Reasons for performing study: The hypometabolic and vasoconstrictive effects of cryotherapy could prevent the development of laminitis. Objectives: To use distal limb cryotherapy to prevent laminitis induced by alimentary carbohydrate overload. Methods: Laminitis was induced in 6 Standardbred horses that had one front limb continuously cooled in an ice/water mixture. Lameness evaluation, blinded lamellar histological grading and analysis for lamellar matrix metalloproteinase-2 (MMP-2) mRNA expression were used to evaluate the severity of laminitis. Results: Cryotherapy was well tolerated and effective in cooling the feet. In each horse no lameness was observed in the treated limbs. Laminitis histology scores in the treated limbs were significantly less than those of the corresponding untreated forelimbs (P<0.05). Laminitis histology scores in the treated limbs were also significantly less than those of the untreated limbs (fore- and hind) as a group (P<0.05). Expression of MMP-2 mRNA in the iced feet was significantly (P<0.05) less than that detected in the untreated feet. Conclusions: Cryotherapy, when applied to one foot, markedly reduced the severity of acute laminitis in this study. We propose that vasoconstriction (preventing delivery of haematogenous trigger factors) and hypometabolism (reduction in lamellar MMP activity) were the primary therapeutic mechanisms. Potential relevance: Although further research is needed, we suggest cryotherapy as a potentially effective prophylactic strategy in horses at risk of developing acute laminitis. [source] | ||||||||||||||||||||||||||||||||||