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Cardiovascular Regulation (cardiovascular + regulation)
Selected AbstractsCardiovascular Regulation through Hypothalamic GABAA Receptors in a Genetic Absence Epilepsy Model in RatEPILEPSIA, Issue 2 2002Rezzan Gülhan Aker Summary: ,Purpose: ,-Aminobutyric acid (GABA) plays a vital role in both central cardiovascular homeostasis and pathogenesis of epilepsy. Epilepsy affects autonomic nervous system functions. In this study, we aimed to clarify the role of GABAA receptors in hypothalamic cardiovascular regulation in a genetically determined animal model of absence epilepsy. Methods: Nonepileptic Wistar rats and genetic absence epilepsy rats from Strasbourg (GAERS) were instrumented with a guide cannula for drug injection and extradural electrodes for EEG recording. After a recovery period, iliac arterial catheters were inserted for direct measurement of mean arterial pressure and heart rate. Bicuculline, a GABAA -receptor antagonist, was injected into the dorsomedial (DMH) or posterior (PH) hypothalamic nuclei of nonepileptic control rats or GAERS. Blood pressure, heart rate, and EEG recordings were performed in conscious unrestrained animals. Results: Bicuculline injections into the hypothalamus produced increases in blood pressure and heart rate of both control rats and GAERS. The DMH group of GAERS showed a twofold increase in the blood pressure and the heart rate compared with those of control rats. Pressor responses to bicuculline, when microinjected into the PH, were similar in the nonepileptic animals and GAERS. Conversely, the amplitude of tachycardic responses to the administration of bicuculline into the PH was significantly higher in GAERS compared with those of control rats. Conclusions: The bicuculline-induced increases in blood pressure and heart rate were more prominent when given in the DMH of GAERS. These results indicate an increased GABAA receptor,mediated cardiovascular response through the DMH in conscious rats with absence epilepsy. [source] The role of caveolin-1 in cardiovascular regulationACTA PHYSIOLOGICA, Issue 2 2009A. Rahman Abstract Caveolae are omega-shaped membrane invaginations present in essentially all cell types in the cardiovascular system, and numerous functions have been ascribed to these structures. Caveolae formation depends on caveolins, cholesterol and polymerase I and transcript release factor-Cavin (PTRF-Cavin). The current review summarizes and critically discusses the cardiovascular phenotypes reported in caveolin-1-deficient mice. Major changes in the structure and function of heart, lung and blood vessels have been documented, suggesting that caveolae play a critical role at the interface between blood and surrounding tissue. According to an emerging paradigm, many of these changes are secondary to uncoupling of endothelial nitric oxide synthase. Thus, nitric oxide synthase not only synthesizes more nitric oxide in the absence of caveolin-1, but also more superoxide with potential pathogenic consequences. It is further argued that the vasodilating drive from increased nitric oxide production in caveolin-1-deficient mice is balanced by changes in the vascular media that favour increased dynamic resistance regulation. Harnessing the therapeutic opportunities buried in caveolae, while challenging, could expand the arsenal of treatment options in cancer, lung disease and atherosclerosis. [source] Cardiovascular Regulation through Hypothalamic GABAA Receptors in a Genetic Absence Epilepsy Model in RatEPILEPSIA, Issue 2 2002Rezzan Gülhan Aker Summary: ,Purpose: ,-Aminobutyric acid (GABA) plays a vital role in both central cardiovascular homeostasis and pathogenesis of epilepsy. Epilepsy affects autonomic nervous system functions. In this study, we aimed to clarify the role of GABAA receptors in hypothalamic cardiovascular regulation in a genetically determined animal model of absence epilepsy. Methods: Nonepileptic Wistar rats and genetic absence epilepsy rats from Strasbourg (GAERS) were instrumented with a guide cannula for drug injection and extradural electrodes for EEG recording. After a recovery period, iliac arterial catheters were inserted for direct measurement of mean arterial pressure and heart rate. Bicuculline, a GABAA -receptor antagonist, was injected into the dorsomedial (DMH) or posterior (PH) hypothalamic nuclei of nonepileptic control rats or GAERS. Blood pressure, heart rate, and EEG recordings were performed in conscious unrestrained animals. Results: Bicuculline injections into the hypothalamus produced increases in blood pressure and heart rate of both control rats and GAERS. The DMH group of GAERS showed a twofold increase in the blood pressure and the heart rate compared with those of control rats. Pressor responses to bicuculline, when microinjected into the PH, were similar in the nonepileptic animals and GAERS. Conversely, the amplitude of tachycardic responses to the administration of bicuculline into the PH was significantly higher in GAERS compared with those of control rats. Conclusions: The bicuculline-induced increases in blood pressure and heart rate were more prominent when given in the DMH of GAERS. These results indicate an increased GABAA receptor,mediated cardiovascular response through the DMH in conscious rats with absence epilepsy. [source] Cardiovascular effects of noradrenaline microinjected into the dorsal periaqueductal gray area of unanaesthetized ratsEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2005Gislaine Garcia Pelosi Abstract The periaqueductal grey area (PAG) is a mesencephalic region that is involved in the modulation of cardiovascular changes associated with behavioural responses. Among the neurotransmitters present in the PAG, noradrenaline (NA) is also known to be involved in central nervous system cardiovascular regulation. In the present study we report the cardiovascular effects of the microinjection of NA into the dorsal portion of the PAG (dPAG) of unanaesthetized rats and the peripheral mechanism involved in their mediation. Injection of NA in the dPAG of unanaesthetized rats evoked a dose-dependent pressor response accompanied by bradycardia. The magnitude of the pressor responses was higher at more rostral sites in the dPAG and decreased when NA was injected into the caudal portion of the dPAG. The responses to NA were markedly reduced in urethane-anaesthetized rats. The pressor response was potentiated by i.v. pretreatment with the ganglion blocker pentolinium and blocked by i.v. pretreatment with the vasopressin antagonist dTyr(CH2)5(Me)AVP. The results suggest that activation of noradrenergic receptors within the dPAG can evoke pressor responses, which are mediated by acute vasopressin release. [source] Transgenic Animals in Cardiovascular Disease ResearchEXPERIMENTAL PHYSIOLOGY, Issue 6 2000Michael Bader Worldwide, the highest morbidity and mortality results from such cardiovascular diseases as hypertension, myocardial infarction, cardiac and renal failure, as well as stroke. Since the cardiovascular system and its regulation is quite complex, study of these disorders has been grossly limited to whole organism models. As a result, in recent years, transgenic technology has played a significant role in the discovery of specific gene products for cardiovascular regulation and disease aetiology. Genetic manipulation in rats and mice has altered the expression of numerous genes. In this review, some of the important new genetically modified animals (i.e. transgenic models) with alterations in hormone and second messenger systems involved in cardiovascular regulation are summarized. [source] Stress Response of Prolactin-Releasing Peptide Knockout Mice as to Glucocorticoid SecretionJOURNAL OF NEUROENDOCRINOLOGY, Issue 6 2010A. Mochiduki Prolactin-releasing peptide (PrRP) is known to have functions in prolactin secretion, stress responses, cardiovascular regulation and food intake suppression. In addition, PrRP-knockout (KO) male mice show obesity from the age of 22 weeks and increase their food intake. The plasma concentrations of insulin, leptin, cholesterol and triglyceride are also increased in obese PrRP-KO mice. Fatty liver, hypertrophied white adipose tissue, decreased uncoupling protein 1 mRNA expression in brown adipose tissue and glucose intolerance were observed in obese PrRP-KO mice. As we reported previously, PrRP stimulates corticotrophin-releasing factor and regulates the hypothalamic-pituitary-adrenal axis. Therefore, it is speculated that PrRP regulates both food intake and metabolism as a stress responses. In the present study, we compared blood glucose and plasma glucocorticoid concentrations in PrRP-KO mice, and found that PrRP-KO mice showed higher concentrations of blood glucose and corticosterone compared to wild-type mice after restraint stress. By contrast, there were no difference in c-Fos expression in the paraventricular hypothalamic nucleus and plasma adrenocorticotrophic hormone concentrations between the two groups. These results suggest that the different stress responses as to glucocorticoid secretion may be induced by different responses of the adrenal glands between wild-type and PrRP-KO mice. Thus, we conclude that PrRP-KO mice become obese as a result of increased food intake, a change in metabolism, and abnormal stress responses as to glucose concentration and glucocorticoid secretion. [source] Adrenomedullin Acts in the Rat Paraventricular Nucleus to Decrease Blood PressureJOURNAL OF NEUROENDOCRINOLOGY, Issue 5 2001P. M. Smith Abstract Adrenomedullin is a recently discovered peptide involved in the control of fluid and electrolyte homeostasis and cardiovascular function through peripheral and central nervous system actions. The present study was undertaken to examine the cardiovascular effects of adrenomedullin microinjection directly into the paraventricular nucleus (PVN). Microinjection of adrenomedullin into the PVN of urethane anaesthetized male Sprague-Dawley rats resulted in site-specific, repeatable decreases in blood pressure. These hypotensive effects were found to be dose related, and were not mediated by activation of calcitonin gene-related peptide receptors. These data suggest that adrenomedullin influences cardiovascular regulation through receptor mediated actions at the PVN of the hypothalamus. [source] Variations in the Thickness and Composition of the Skin of the GiraffeTHE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 9 2010Farzana Sathar Abstract This study examined the skin of two 1- to 2-year-old male giraffes and one adult male, determining skin thickness and histological structure with reference to it functioning as a component of the features required for the maintenance of blood pressure, dermal armor, or thermoregulation. It has been argued that a tight skin surrounding the extremities of the giraffe aids in the movement of fluid against gravity, hence preventing pooling of blood and tissue fluid (edema), but the skin has also been implicated in the thermoregulatory capacities and defensive anatomy of many mammalian species. In one of the younger giraffes, one-half of the skin was analyzed from which close to 170 sites were measured. In the other young and adult giraffes, spot tests to confirm the pattern observed in the fully analyzed individual were undertaken. It was discovered that the skin varied in thickness across the entire body and within regions of the body. Histological evaluation revealed that the skin was mostly collagenous, although interesting patterns of elastic fiber densities were also apparent. The skin in the neck and legs exhibited a morphology that may assist in cardiovascular regulation of blood flow to and from the head and legs, and the skin of the trunk and anterior neck has the possibility of functioning in a protective role. The analyses performed could not add any new data regarding the thermoregulatory role already described for giraffe skin. Anat Rec 293:1615,1627, 2010. © 2010 Wiley-Liss, Inc. [source] Human head exposure to a 37 Hz electromagnetic field: Effects on blood pressure, somatosensory perception, and related parametersBIOELECTROMAGNETICS, Issue 3 2004Sergio Ghione Abstract Previous studies have shown that exposure to an electromagnetic field (EMF) of 37 Hz at a flux density of 80 ,T peak enhances nociceptive sensitivity in mice. Here we examined the effects on pain sensitivity and some indexes of cardiovascular regulation mechanisms in humans by measuring electrical cutaneous thresholds, arterial blood pressure, heart rate and its variability, and stress hormones. Pain and tolerance thresholds remained unchanged after sham exposure but significantly decreased after electromagnetic exposure. Systolic blood pressure was significantly higher during electromagnetic exposure and heart rate significantly decreased, both during sham and electromagnetic exposure, while the high frequency (150,400 mHz) component of heart rate variability, which is an index of parasympathetic activity, increased as expected during sham exposure but remained unchanged during electromagnetic exposure. Cortisol significantly decreased during sham exposure only. These results show that exposure to an EMF of 37 Hz also alters pain sensitivity in humans and suggest that these effects may be associated with abnormalities in cardiovascular regulation. Bioelectromagnetics 25:167,175, 2004. © 2004 Wiley-Liss, Inc. [source] Geomagnetic field effect on cardiovascular regulationBIOELECTROMAGNETICS, Issue 2 2004Juraj Gmitrov Abstract The goal of the present research was try to explain the physiological mechanism for the influence of the geomagnetic field (GMF) disturbance, reflected by the indices of the geomagnetic activity (K, Kp, Ak, and Ap indices), on cardiovascular regulation. One hundred forty three experimental runs (one daily) comprising 50 min hemodynamic monitoring sequences were carried out in rabbits sedated by pentobarbital infusion (5 mg/kg/h). We examined the arterial baroreflex effects on the short term blood pressure and heart rate (HR) variabilities reflected by the standard deviation (SD) of the average values of the mean femoral arterial blood pressure (MAP) and the HR. Baroreflex sensitivity (BRS) was estimated from blood pressure/HR response to intravenous (i.v.) bolus injections of vasoconstrictor (phenylephrine) and vasodilator (nitroprusside) drugs. We found a significant negative correlation of increasing GMF disturbance (Kp) with BRS (P,=,0.008), HR SD (P,=0.022), and MAP SD (P,=,0.002) signifying the involvement of the arterial baroreflex mechanism. The abrupt change in geomagnetic disturbance from low (K,=,0) to high (K,=,4,5) values was associated with a significant increase in MAP (83,±,5 vs. 99,±,5 mm Hg, P,=,0.045) and myocardial oxygen consumption, measured by MAP and HR product (24100,±,1800 vs. 31000,±,2500 mm Hg,·,bpm, P,=,0.034), comprising an additional cardiovascular risk. Most likely, GMF affects brainstem and higher neural cardiovascular regulatory centers modulating blood pressure and HR variabilities associated with the arterial baroreflex. Bioelectromagnetics 25:92,101, 2004. © 2004 Wiley-Liss, Inc. [source] Non-invasive assessment of cardioregulatory autonomic functions in children with epilepsyACTA NEUROLOGICA SCANDINAVICA, Issue 6 2007H. L. El-Sayed Objectives ,, We aimed to evaluate the interictal cardiovascular autonomic functions in pediatric patients with idiopathic epilepsy, both partial and generalized. Materials and methods ,, The study included 25 patients with idiopathic epilepsy and 50 control subjects. Patients underwent five standardized clinical cardiovascular reflex autonomic tests [resting heart rate (HR), HR response to deep breathing and to Valsalva maneuver, the 30:15 ratio of HR response to standing, and blood pressure response to standing], as well as a 12 lead surface electrocardiogram. Heart rate variability (HRV) was tested via 24-h Holter monitoring and the time domain parameters (SDNN, PNN50, rMSDD) were assessed. Excretion of vanillyl mandelic acid and metanephrine was measured in 24-h urine collection. Results ,, Clinical reflex autonomic tests showed mild dysfunction in 8%, moderate dysfunction in 44% and severe dysfunction in 4% of patients. The HRV parameter, SDNN, was reduced in all age groups, while rMSDD and PNN50 were reduced only in the older age group. Metanephrine levels were significantly reduced in the patients group. Patients with uncontrolled epilepsy had a significantly higher frequency of autonomic dysfunction as assessed by clinical scoring. Conclusion ,, Cardiac autonomic dysfunction is not uncommon in pediatric patients with epilepsy. Altered cardiovascular regulation seems to be related to the epilepsy itself rather than to the characteristics of the disorder. [source] Does It Make Sense To Develop New Centrally Acting Cardiovascular Drugs?CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 12 2001P Bousquet SUMMARY 1. The autonomic nervous system plays a pivotal role in modulating all the components of the cardiovascular regulation. Therefore, one can assume that drugs targeting this system may be useful in the management of several cardiovascular diseases. 2. Drugs acting on central nervous system centres seem to be modulators rather than blockers; as such, they are expected to preserve the contraregulatory processes and to generate only a few side effects. 3. Because the sympathetic nervous system is largely involved in the regulation of vasomotor tone, centrally acting antihypertensive drugs were developed first. 4. Recently, new leader compounds selective for non- adrenergic imidazoline recepetors have been synthetized. Although such drugs have no capacity to activate ,2 -adrenoceptors, they have been proven to be hypotensive. These drugs are expected to be even better tolerated than the currently available centrally active drugs. They may also have additional beneficial effects. 5. Here, the experimental evidence suggesting that such drugs may be useful in the management of some cardiac arrhythmias and/or left ventricular dysfunction will be reviewed. [source] Role Of Nitric Oxide On Pressor Mechanisms Within The Dorsomedial And Rostral Ventrolateral Medulla In Anaesthetized CatsCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 3 2001Shu-Ying Chen SUMMARY 1. The role of nitric oxide (NO) in central cardiovascular regulation and the correlation between NO and glutamate-induced mechanisms is not clear. Microinjection of glutamate (3 nmol/ 30 nL) into dorsomedial medulla (DM) and rostral ventrolateral medulla (RVLM) increased arterial blood pressure (BP) and sympathetic vertebral nerve activity (VNA). Thus, in the present study, we examined the modulation by NO of glutamate-induced pressor responses in the DM and RVLM of cats. 2. Histochemical methods using nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd) as a marker to stain neurons containing NO synthase (NOS), showed positive findings of NOS in both the DM and RVLM. 3. Microinjection of NG -nitro- L -arginine methyl ester (L -NAME), a NOS inhibitor, into the DM or RVLM did not alter resting BP and VNA, but it did cause a dose-dependent attenuation of glutamate-induced pressor responses. Interestingly, the increase in NO levels that resulted from pretreatment with L -arginine (L -Arg) or sodium nitroprusside (SNP) did not alter resting BP and VNA, but still inhibited glutamate-induced pressor responses in the DM and RVLM in a dose-dependent manner. 4. We also examined whether NO modulated the pressor responses induced by activation of different excitatory amino acid receptors. N -Methyl- D -aspartate (NMDA) and , -amino-3-hydroxy-5-methyl-4-isoxazole proprionic acid (AMPA) were used. Consistent with the results from the initial glutamate studies, we observed that not only L -NAME, but also L -Arg and SNP attenuated pressor responses induced by NMDA and AMPA. No difference was found between the effects of NO on NMDA- and AMPA-induced pressor responses. 5. To investigate the possibility of a loss of agonist selectivity, the effects of D -2-amino-5-phosphonovalerate (D -AP5) and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) on AMPA and NMDA responses in the DM were examined. The results showed that CNQX did not alter NMDA-induced pressor responses, while D -AP5 failed to alter AMPA-induced responses. 6. Our results suggest that activation of the glutamate-induced pressor mechanism is regulated by changes in NO levels in the DM and RVLM. This implies that NO may play a permissive role to allow operation of the glutamate-activation mechanism. [source] Area Postrema And Sympathetic Nervous System Effects Of Vasopressin And Angiotensin IICLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2000Eileen M Hasser SUMMARY 1. Precise control over the cardiovascular system requires the integration of both neural and humoral signals related to blood volume and blood pressure. Humoral signals interact with neural systems, modulating their control over the efferent mechanisms that ultimately determine the level of pressure and volume. 2. Peptide hormones such as angiotensin (Ang)II and arginine vasopressin (AVP) act through circumventricular organs (CVO) to influence cardiovascular regulation. 3. The area postrema (AP), a CVO in the brainstem, mediates at least some of the central actions of these peptides. Vasopressin appears to act in the AP to cause sympathoinhibition and a shift in baroreflex control of the sympathetic nervous system (SNS) to lower pressures. These effects of AVP and the AP appear to be mediated by ,2 -adrenoceptor and glutamatergic mechanisms in the nucleus tractus solitarius. 4. In contrast to AVP AngII has effects in the AP to blunt baroreflex control of heart rate and cause sympathoexcitation. The effects of chronic AngII to increase activity of the SNS may be due to AP-dependent activation of neurons in the rostral ventrolateral medulla. [source] | |||||||||||||