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Renal Blood Flow (renal + blood_flow)

Distribution by Scientific Domains

Medical Sciences	81%
Life Sciences	18%

Selected Abstracts

RGS4 Controls Renal Blood Flow and Inhibits Cyclosporine-Mediated Nephrotoxicity

AMERICAN JOURNAL OF TRANSPLANTATION, Issue 2 2010
A. Siedlecki
Calcineurin inhibitors (CNI) are powerful immunomodulatory agents that produce marked renal dysfunction due in part to endothelin-1-mediated reductions in renal blood flow. Ligand-stimulated Gq protein signaling promotes the contraction of smooth muscle cells via phospholipase C,-mediated stimulation of cytosolic calcium release. RGS4 is a GTPase activating protein that promotes the deactivation of Gq and Gi family members. To investigate the role of G protein-mediated signaling in the pathogenesis of CNI-mediated renal injury, we used mice deficient for RGS4 (rgs4,/,). Compared to congenic wild type control animals, rgs4,/, mice were intolerant of the CNI, cyclosporine (CyA), rapidly developing fatal renal failure. Rgs4,/, mice exhibited markedly reduced renal blood flow after CyA treatment when compared to congenic wild type control mice as measured by magnetic resonance imaging (MRI). Hypoperfusion was reversed by coadministration of CyA with the endothelin antagonist, bosentan. The MAPK/ERK pathway was activated by cyclosporine administration and was inhibited by cotreatment with bosentan. These results show that endothelin-1-mediated Gq protein signaling plays a key role in the pathogenesis of vasoconstrictive renal injury and that RGS4 antagonizes the deleterious effects of excess endothelin receptor activation in the kidney. [source]

Neural Regulation Of Renal Blood Flow: A Re-Examination

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 12 2000
Simon C Malpas
SUMMARY 1. The importance of renal sympathetic nerve activity (RSNA) in the regulation of renal function is well established. However, it is less clear how the renal vasculature responds to the different mean levels and patterns of RSNA. While many studies have indicated that small to moderate changes in RSNA preferentially regulate renin secretion or sodium excretion and only large changes in RSNA regulate renal blood flow (RBF), other experimental evidence suggests that small changes in RSNA can influence RBF 2. When RSNA has been directly measured in conjunction with RBF, it appears that a range of afferent stimuli can induce reflex changes in RBF. However, many studies in a variety of species have measured RBF only during stimuli designed to reflexly increase or decrease sympathetic activity, but have not recorded RSNA. While this approach can be informative, it is not definitive because the ability of the vasculature to respond to RSNA may, in part, reflect the resting level of RSNA and, therefore, the vasoconstrictive state of the vasculature under the control conditions. 3. Further understanding of the control of RBF by RSNA has come from studies that have analysed the underlying rhythms in sympathetic nerve activity and their effect on the cardiovascular system. These studies show that the frequency,response characteristic of the renal vasculature is such that higher frequency oscillations in RSNA (above 0.6 Hz) contribute to setting the mean level of RBF. In comparison, lower frequency oscillations in RSNA can induce cyclic vasoconstriction and dilation in the renal vasculature, thus inducing oscillations in RBF. 4. In summary, the present review discusses the neural control of RBF, summarizing evidence in support of the hypothesis that RBF is under the influence of RSNA across the full range of RSNA. [source]

Intrauterine growth restriction reduces nephron number and renal excretory function in newborn piglets,

ACTA PHYSIOLOGICA, Issue 2 2002
R. Bauer
ABSTRACT To examine the effects of intrauterine growth restriction on nephron number, renal circulation, and renal excretory functions in newborns, studies were conducted on 1-day-old anaesthetized piglets, divided into normal weight (n = 6) and intrauterine growth restricted (n = 6) piglets. Renal blood flow was measured by coloured microspheres, glomerular filtration rate was measured by inulin clearance, and osmotic clearance and fractional sodium excretion were calculated. In addition, an estimation of the nephron number was performed by counting representative glomerular numbers in microscopic sections. Newborn intrauterine growth restricted piglets exhibited a reduced glomerular filtration rate and osmotic clearance (P < 0.05), whereas renal blood flow and the filtration fraction as well as fractional sodium excretion were similar in normal weight and intrauterine growth restricted piglets. The nephron number was markedly reduced in intrauterine growth restricted piglets even if the nephron number was related to body weight (P < 0.01). There was a positive correlation between nephron number and glomerular filtration rate (r = 0.69, P < 0.05). Reduced glomerular filtration rate of newborn intrauterine growth restricted piglets is associated with a reduced nephron number. Thus, at birth, compensatory response of renal function due to nephron deficit does not exist in intrauterine growth restricted piglets. [source]

MR determination of glomerular filtration rate in subjects with solitary kidneys in comparison to clinical standards of renal function: feasibility and preliminary report,

CONTRAST MEDIA & MOLECULAR IMAGING, Issue 2 2009
Richard W. Katzberg
Abstract This study was conducted to demonstrate the feasibility of quantifying single kidney glomerular filtration rate (skGFR) by magnetic resonance (MR) by comparison to the clinical estimates of GFR in volunteer subjects with a single kidney. Seven IRB-approved subjects with a solitary kidney, stable serum creatinine (SCr) and a 24,h creatinine clearance (CrCl) volunteered to undergo an MR examination that determined renal extraction fraction (EF) with a breathhold inversion recovery echo planar pulse sequence and renal blood flow with a velocity encoded phase imaging sequence. The product of EF and blood flow determines GFR. These values were compared with the 24,h CrCl, estimated GFR by the modification of diet in renal disease (MDRD) regression analysis and the Cockroft,Gault (CG) determination of CrCl. The mean and standard deviation of differences between the MR GFR, MDRD and CG vs the 24,h CrCl were 12.3,±,35.7, ,8.9,±,18.5 and 1.2,±,19.6, respectively. The Student t -test showed that none of the mean differences were statistically significant between techniques. This clinical investigation shows that MR can be used for skGFR determination in human subjects with comparable values to those derived from clinically used serum-based GFR estimation techniques. Copyright © 2009 John Wiley & Sons, Ltd. [source]

Nitric oxide, superoxide and renal blood flow autoregulation in SHR after perinatal L -arginine and antioxidants

ACTA PHYSIOLOGICA, Issue 4 2007
M. P. Koeners
Abstract Aim:, Nitric oxide (NO) and superoxide are considered to be regulatory in renal blood flow (RBF) autoregulation, and hence may contribute to development of hypertension. To extend our previous observations that dynamic NO release is impaired in the spontaneously hypertensive rat (SHR) we investigated, firstly, if superoxide dependency of RBF autoregulation is increased in SHR and, secondly, if the beneficial effect of perinatal supplementation in SHR is partly as a result of early correction of RBF autoregulation. We hypothesized that perinatal supplementation by restoring dynamic NO release and/or decreasing superoxide dependency and would improve life-long blood pressure regulation. Methods:, Autoregulation was studied using stepwise reductions in renal perfusion pressure in anaesthetized male SHR, SHR perinatally supplemented with arginine and antioxidants (SHRsuppl) and Wistar-Kyoto (WKY), prior to and during i.v. N, -nitro- l -arginine (NO synthase inhibitor) or tempol (superoxide dismutase mimetic). Results:, Spontaneously hypertensive rat displayed a wider operating range of RBF autoregulation as compared with WKY (59 ± 4 vs. 33 ± 2 mmHg, respectively; P < 0.01). Perinatal supplementation in SHR decreased mean arterial pressure, renal vascular resistance and the operating range of RBF autoregulation (43 ± 3 mmHg; P < 0.01). In addition autoregulation efficiency decreased. RBF autoregulation characteristics shifted towards those of normotensive WKY. However, dynamic NO release was still impaired and no clear differences in superoxide dependency in RBF autoregulation between groups was observed. Conclusion:, Perinatal supplements shifted RBF autoregulation characteristics of SHR towards WKY, although capacity of the SHRsuppl kidney to modulate NO production to shear stress still seems impaired. The less strictly controlled RBF as observed in perinatally supplemented SHR could result in an improved long-term blood pressure control. This might partly underlie the beneficial effects of perinatal supplementation. [source]

Intrauterine growth restriction reduces nephron number and renal excretory function in newborn piglets,

Sustained increase in arterial blood pressure and vascular resistance induced by infusion of arachidonic acid in rats

ACTA PHYSIOLOGICA, Issue 1 2000
Kirkebø
The haemodynamic responses to arachidonic acid (AA) have been investigated in seven groups of anaesthetized rats. Sodium arachidonate was infused intravenously for 4 or 20 min, and arterial blood pressure was recorded continuously. Cardiac output and organ blood flow were measured by microspheres. Infusion of arachidonate caused first a fast drop in arterial blood pressure, thereafter it increased steadily for 5,15 min towards a pressure about 25 mmHg above control level. The high pressure was maintained for at least 1 h. Repeated infusions of arachidonate gave similar responses. Inhibition of cyclo-oxygenase by indomethacin prevented the initial pressure drop to arachidonate, but not the sustained increase in pressure. Arterial pressure, total vascular resistance and blood flow in the kidneys, adrenals and spleen were significantly reduced, whereas cardiac output was not changed 4 min after start infusion of arachidonate. However, average blood pressure was significantly increased 22 and 35 min after start infusion (from 103.9 ± 2.9 to 128.1 ± 6.1 and 135.8 ± 4.6 mmHg). Mean vascular resistance increased simultaneously (from 3.5 ± 0.2 to 4.7 ± 0.4 and 5.2 ± 0.4 mmHg 100 mL,1), while cardiac output, stroke volume and heart rate were maintained or slightly reduced. The renal blood flow was significantly lowered (from average 4.9 ± 0.1 to 3.3 ± 0.2 and 4.0 ± 0.2 mL min,1). Indomethacin did not prevent the changes in vascular resistance or organ blood flow recorded after 20,35 min. On the other hand, inhibition of both cyclo-oxygenase, lipoxygenase and the cytochrome P450 pathways by eicosatetrayonic acid (ETYA) normalized all haemodynamic parameters. Likewise, the rise in pressure was prevented by 17-octadecynoic acid (17-ODYA), an inhibitor of the cytochrome P450 enzyme activity. Thus, arachidonate infusion caused a transient decrease, and then a sustained increase in arterial pressure and vascular resistance, and a long-lasting reduction in renal blood flow, possibly owing to release of a cytochrome P450 dependent vasoconstrictor metabolite of AA. [source]

Modulation of systemic and renal haemodynamics by ,-opioids in conscious lambs

EXPERIMENTAL PHYSIOLOGY, Issue 5 2006
Wei Qi
The purpose of the present study was to determine the cardiovascular effects of the ,-opioid receptor agonist U-50488H at two stages of postnatal maturation under physiological conditions. Experiments were carried out firstly to define systemic and renal haemodynamic responses to ,-opioid receptor activation and, secondly, to determine whether these effects are altered during postnatal maturation. To investigate whether the responses to U-50488H resulted from receptor-dependent effects, responses to U-50488H were also tested in the presence of the specific ,-opioid receptor antagonist 5,-guanidinonaltrindole (GNTI). Experiments were carried out in two groups of conscious, chronically instrumented lambs aged ,1 and ,6 weeks. Mean arterial pressure, mean venous pressure and renal blood flow (RBF) were measured for 30 min before and 90 min after i.v. injection of U-50488H or vehicle. Heart rate increased in both age groups of lambs within 10 min of U-50488H administration. Mean arterial pressure decreased for 50 min following U-50488H administration at 1 week but, in contrast, increased transiently at 10 min in 6-week-old lambs, returning to control levels by 20 min. In both age groups, there was a sustained decrease in RBF following U-50488H. The aforementioned responses to U-50488H were abolished by pretreatment with GNTI. These data provide the first measurements of systemic and renal haemodynamic responses to ,-opioid receptor activation during postnatal maturation. [source]

Role of nitric oxide in the reflex diuresis in rabbits during pulmonary lymphatic obstruction

EXPERIMENTAL PHYSIOLOGY, Issue 4 2004
K. M. McCormick
The role of nitric oxide in the reflex diuresis in response to pulmonary lymphatic drainage was examined in anaesthetized, artificially ventilated New Zealand White rabbits. Pulmonary lymphatic drainage was obstructed by raising the pressure in a pouch created from the right external jugular vein. Pulmonary lymphatic obstruction resulted in a significant increase in urine flow from an initial control value of 8.9 ± 0.5 ml (10 min),1 to 12.1 ± 0.6 ml (10 min),1 during lymphatic obstruction (mean ±s.e.m.; n= 17, P < 0.001). This increase in urine flow was accompanied by a significant increase in the excretion of sodium. Additionally, renal blood flow remained unchanged during the increase in urine flow caused by lymphatic obstruction. Intravenous infusion of l -NAME, a non-selective inhibitor of nitric oxide synthase (NOS), abolished the reflex diuresis. Furthermore, intraperitoneal administration of the relatively selective neuronal NOS blocker, 7-nitroindazole also abolished the response. It was observed that infusion of a more soluble neuronal NOS blocker, 7-nitroindazole sodium salt (7-NINA), into the renal medulla also abolished the reflex diuresis. These findings suggest that the increase in urine flow in rabbits caused by pulmonary lymphatic obstruction is dependent upon the integrity of neuronal NOS activity within the renal medulla. [source]

Vascular and renal actions of brain natriuretic peptide in man: physiology and pharmacology

FUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 4 2005
Alphons J.H.M. Houben
Abstract During the last decade brain natriuretic peptide (BNP) has received increasing attention as a potential marker of cardiovascular disease. BNP may act as a compensating mechanism in cardiovascular diseases in order to reduce preload. However, the increase in endogenous BNP is often not sufficient to compensate for volume overload in diseases like established hypertension and heart failure. The reported hemodynamic and renal effects of BNP in man differ largely between studies, because of differences in design and doses of BNP employed. In the pharmacological range, BNP has clear blood pressure and afterload lowering effects, and in the kidney blood flow and filtration is increased with concomitant natriuresis and diuresis. While in the physiological range BNP does not affect blood pressure and reduces preload only, and induces natriuresis/diuresis without changes in renal blood flow and filtration. There is increasing evidence from vascular studies that BNP preferentially acts on the venous system resulting in preload reduction, in contrast to atrial natriuretic peptide which acts preferentially on the arterial system to reduce afterload. This review summarizes our current understanding of BNP, and discuss its regulation and mechanisms of action on the vasculature and the kidneys. [source]

Acute kidney injury in cirrhosis,

HEPATOLOGY, Issue 6 2008
Guadalupe Garcia-Tsao
Acute renal failure (ARF), recently renamed acute kidney injury (AKI), is a relatively frequent problem, occurring in approximately 20% of hospitalized patients with cirrhosis. Although serum creatinine may underestimate the degree of renal dysfunction in cirrhosis, measures to diagnose and treat AKI should be made in patients in whom serum creatinine rises abruptly by 0.3 mg/dL or more (,26.4 ,mol/L) or increases by 150% or more (1.5-fold) from baseline. The most common causes of ARF (the term is used interchangeably with AKI) in cirrhosis are prerenal azotemia (volume-responsive prerenal AKI), acute tubular necrosis, and hepatorenal syndrome (HRS), a functional type of prerenal AKI exclusive of cirrhosis that does not respond to volume repletion. Because of the progressive vasodilatory state of cirrhosis that leads to relative hypovolemia and decreased renal blood flow, patients with decompensated cirrhosis are very susceptible to developing AKI with events associated with a decrease in effective arterial blood volume. HRS can occur spontaneously but is more frequently precipitated by events that worsen vasodilatation, such as spontaneous bacterial peritonitis. Conclusion: Specific therapies of AKI depend on the most likely cause and mechanism. Vasoconstrictors are useful bridging therapies in HRS. Ultimately, liver transplantation is indicated in otherwise reasonable candidates in whom AKI does not resolve with specific therapy. (HEPATOLOGY 2008;48:2064-2077.) [source]

Acute renal failure in patients with cirrhosis: Perspectives in the age of MELD

HEPATOLOGY, Issue 2 2003
Richard Moreau
In patients with cirrhosis, acute renal failure is mainly due to prerenal failure (caused by renal hypoperfusion) and tubular necrosis. The main causes of prerenal failure are "true hypovolemia" (induced by hemorrhage or gastrointestinal or renal fluid losses), sepsis, or type 1 hepatorenal syndrome (HRS). The frequency of prerenal failure due to the administration of nonsteroidal anti-inflammatory drugs or intravascular radiocontrast agents is unknown. Prerenal failure is rapidly reversible after restoration of renal blood flow. Treatment is directed to the cause of hypoperfusion, and fluid replacement is used to treat most cases of "non-HRS" prerenal failure. In patients with type 1 HRS with very low short-term survival rate, liver transplantation is the ideal treatment. Systemic vasoconstrictor therapy (with terlipressin, noradrenaline, or midodrine [combined with octreotide]) may improve renal function in patients with type 1 HRS waiting for liver transplantation. MARS (for molecular adsorbent recirculating system) and the transjugular intrahepatic portosystemic shunt may also improve renal function in these patients. In patients with cirrhosis, acute tubular necrosis is mainly due to an ischemic insult to the renal tubules. The most common condition leading to ischemic acute tubular necrosis is severe and sustained prerenal failure. Little is known about the natural course and treatment (i.e., renal replacement therapy) of cirrhosis-associated acute tubular necrosis. [source]

Assessment of renal function with color Doppler ultrasound in autosomal dominant polycystic kidney disease

INTERNATIONAL JOURNAL OF UROLOGY, Issue 3 2001
Akira Kondo
Abstract Background: Measurement of renal blood flow by color Doppler ultrasound is useful for assessment of renal function in a variety of renal disorders. In autosomal dominant polycystic kidney disease (ADPKD), however, it might be difficult to visualize interlobar arteries because of deformity of renal structure. To evaluate the usefulness of color Doppler in ADPKD, parameters determined by blood flow examination were compared with the results of ordinal renal function tests. Methods: Twenty-one patients with ADPKD were examined by color Doppler ultrasound measurement. In each patient, 10 interlobar arteries in both kidneys were investigated. Minimum blood flow velocity (Vmin), maximum blood flow velocity (Vmax), mean blood flow velocity (Vmean), acceleration, resistive index and pulsatility index were measured in relation to the results of creatinine clearance, serum creatinine, blood urea nitrogen and 15 and 120 min values of the phenolsulfonphthalein test. Results: In all patients, interlobar arteries were able to be visualized and blood-flow profile was measured. Although variations of Vmin, Vmax, Vmean and acceleration were relatively large, the resistive index and pulsatility index varied little in each kidney. Mean values of Vmin (P < 0.005), Vmean (P < 0.05), resistive index (P < 0.005) and pulsatility index (P < 0.005) were well correlated to creatinine clearance with statistical significance. Conclusions: In ADPKD, color Doppler ultrasound measurement is a useful method for assessment of renal function and could be used for monitoring the dynamic state of renal blood flow as a non-invasive technique. [source]

Dopamine increases renal oxygenation: a clinical study in post-cardiac surgery patients

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 2 2010
BENGT REDFORS
Background: Imbalance of the renal medullary oxygen supply/demand relationship can cause ischaemic acute renal failure (ARF). The use of dopamine for prevention/treatment of ischaemic ARF has been questioned. It has been suggested that dopamine may increase renal oxygen consumption (RVO2) due to increased solute delivery to tubular cells, which may jeopardise renal oxygenation. Information on the effects of dopamine on renal perfusion, filtration and oxygenation in man is, however, lacking. We evaluated the effects of dopamine on renal blood flow (RBF), glomerular filtration rate (GFR), RVO2 and renal O2 demand/supply relationship, i.e. renal oxygen extraction (RO2Ex). Methods: Twelve uncomplicated, mechanically ventilated and sedated post-cardiac surgery patients with pre-operatively normal renal function were studied. Dopamine was sequentially infused at 2 and 4 ug/kg/min. Systemic haemodynamics were evaluated by a pulmonary artery catheter. Absolute RBF was measured using two independent techniques: by the renal vein thermodilution technique and by infusion clearance of paraaminohippuric acid (PAH), with a correction for renal extraction of PAH. The filtration fraction (FF) was measured by the renal extraction of 51Cr-EDTA. Results: Neither GFR, tubular sodium reabsorption nor RVO2 was affected by dopamine, which increased RBF (45,55%) with both methods, decreased renal vascular resistance (30,35%), FF (21,26%) and RO2Ex (28,34%). The RBF/CI ratio increased with dopamine. Dopamine decreased renal PAH extraction, suggestive of a flow distribution to the medulla. Conclusions: In post-cardiac surgery patients, dopamine increases the renal oxygenation by a pronounced renal pre-and post-glomerular vasodilation with no increases in GFR, tubular sodium reabsorption or renal oxygen consumption. [source]

Low-dose vasopressin increases glomerular filtration rate, but impairs renal oxygenation in post-cardiac surgery patients

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 8 2009
G. BRAGADOTTIR
Background: The beneficial effects of vasopressin on diuresis and creatinine clearance have been demonstrated when used as an additional/alternative therapy in catecholamine-dependent vasodilatory shock. A detailed analysis of the effects of vasopressin on renal perfusion, glomerular filtration, excretory function and oxygenation in man is, however, lacking. The objective of this pharmacodynamic study was to evaluate the effects of low to moderate doses of vasopressin on renal blood flow (RBF), glomerular filtration rate (GFR), renal oxygen consumption (RVO2) and renal oxygen extraction (RO2Ex) in post-cardiac surgery patients. Methods: Twelve patients were studied during sedation and mechanical ventilation after cardiac surgery. Vasopressin was sequentially infused at 1.2, 2.4 and 4.8 U/h. At each infusion rate, systemic haemodynamics were evaluated by a pulmonary artery catheter, and RBF and GFR were measured by the renal vein thermodilution technique and by renal extraction of 51chromium,ethylenediaminetetraacetic acid, respectively. RVO2 and RO2Ex were calculated by arterial and renal vein blood samples. Results: The mean arterial pressure was not affected by vasopressin while cardiac output and heart rate decreased. RBF decreased and GFR, filtration fraction, sodium reabsorption, RVO2, RO2Ex and renal vascular resistance increased dose-dependently with vasopressin. Vasopressin exerted direct antidiuretic and antinatriuretic effects. Conclusions: Short-term infusion of low to moderate, non-hypertensive doses of vasopressin induced a post-glomerular renal vasoconstriction with a decrease in RBF and an increase in GFR in post-cardiac surgery patients. This was accompanied by an increase in RVO2, as a consequence of the increases in the filtered tubular load of sodium. Finally, vasopressin impaired the renal oxygen demand/supply relationship. [source]

Assessment of renal circulation in small for gestational age and appropriate for gestational age term newborns: A prospective study

JOURNAL OF CLINICAL ULTRASOUND, Issue 4 2008
Hana Kolarovszka
Abstract Purpose To compare selected parameters of renal circulation between small for gestational age (SGA) and appropriate for gestational age (AGA) newborns. Methods Fifty-two SGA and 100 AGA term newborns were examined. The size of the kidneys were measured, and renal blood flow in the central and intraparenchymal renal arteries were assessed via Doppler sonography. Peak systolic velocity (PSV), end diastolic velocity (EDV), mean blood flow velocity (V mean), resistance index (RI), and pulsatility index (PI) were determined and compared between the groups. Results No statistically significant differences in the velocity parameters were found between SGA and AGA infants in central renal arteries. Slightly higher RIs and PIs were seen in AGA newborns (RI, 0.76 ± 0.13 versus 0.78 ± 0.06 [p < 0.05]; PI, 1.65 ± 0.54 versus 1.84 ± 0.46 [p < 0.05]). There were statistically significant differences between the groups in all measured parameters in intraparenchymal arteries (RI, 0.57 ± 0.11 versus 0.63 ± 0.05 [p < 0.001]; PI, 0.89 ± 0.26 versus 1.09 ± 0.16 [p < 0.001]) except PSV (7.11 ± 1.55 versus 7.14 ± 0.81 cm/s [p > 0.05]). Conclusion Based on our findings, we suggest that renal circulation is not negatively influenced by intrauterine growth restriction in SGA neonates compared with AGA newborns. © 2007 Wiley Periodicals, Inc. J Clin Ultrasound, 2008 [source]

Power Doppler sonography of the kidney: Effect of Valsalva's maneuver

JOURNAL OF CLINICAL ULTRASOUND, Issue 7 2001
Ryuichi Takano MD
Abstract Purpose It has been reported that an intra-abdominal pressure (IAP) above 15 mm Hg may cause oliguria and that an IAP above 25 mm Hg may cause anuria. Because Valsalva's maneuver yields an IAP exceeding 180 mm Hg, it is presumed to affect renal perfusion. We evaluated the ability of power Doppler sonography to depict the changes in renal blood flow during Valsalva's maneuver. Methods Seven healthy men aged 21,24 years and 1 50-year-old man with massive ascites participated in the study. With each healthy subject lying in a supine position, longitudinal power Doppler sonograms of the kidney were obtained and analyzed semiquantitatively during Valsalva's maneuver. Also, in the patient with massive ascites, power Doppler sonography was performed before and after paracentesis. Results Along with an increase in IAP, monitored as expiratory pressure during Valsalva's maneuver, power Doppler signals decreased as indicated by both visual impression and computer scores. In the patient with massive ascites, signal intensity increased after paracentesis. Conclusions Our results demonstrated that an increase in IAP within the physiologic range affects renal perfusion and that power Doppler sonography depicts semiquantitatively the change in renal blood flow. © 2001 John Wiley & Sons, Inc. J Clin Ultra- 29:384,388, 2001. [source]

Effects of Norepinephrine and Combined Norepinephrine and Fenoldopam Infusion on Systemic Hemodynamics and Indices of Renal Function in Normotensive Neonatal Foals

JOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 5 2008
A.R. Hollis
Background: Norepinephrine increases arterial blood pressure but may have adverse effects on renal blood flow. Fenoldopam, a dopamine-1 receptor agonist, increases urine output in normotensive foals. The combination of norepinephrine and fenoldopam may lead to improved renal perfusion compared with an infusion of norepinephrine alone. The combined effects of these drugs have not been reported in the horse. Hypothesis: Norepinephrine will alter the hemodynamic profile of foals without affecting renal function. Addition of fenoldopam will change the renal profile during the infusions without changing the hemodynamic profile. Animals: Five conscious pony foals. Methods: Each foal received norepinephrine (0.3 ,g/kg/min), combined norepinephrine (0.3 ,g/kg/min) and fenoldopam (0.04 ,g/kg/min), and a control dose of saline in a masked, placebo-controlled study. Heart rate (HR), arterial blood pressure (direct), and cardiac output (lithium dilution) were measured, and systemic vascular resistance (SVR), stroke volume, cardiac index (CI), and stroke volume index were calculated. Urine output, creatinine clearance, and fractional excretion of electrolytes were measured. Results: Norepinephrine and a combined norepinephrine and fenoldopam infusion increased arterial blood pressure, SVR, urine output, and creatinine clearance and decreased HR and CI compared with saline. The combination resulted in higher HR and lower arterial blood pressure than norepinephrine alone. Conclusions and Clinical Importance: Norepinephrine might be useful for hypotensive foals, because in normal foals, this infusion rate increases SVR without negatively affecting renal function (creatinine clearance increased). Fenoldopam does not provide additional benefit to renal function. These findings warrant further investigation. [source]

Changes in renal hemodynamics and urodynamics in rats with chronic hyperoxaluria and after acute oxalate infusion: Role of free radicals

NEUROUROLOGY AND URODYNAMICS, Issue 2 2003
Ho-Shiang Huang
Abstract Aims The aim of this study was to evaluate possible changes in renal hemodynamic and urodynamic parameters in rats with chronic hyperoxaluria and after acute oxalate challenge. We also evaluated the possible association between free radical (FR) production, hyperoxaluria, and calcium oxalate (CaOx) calculi formation. Methods Chronic hyperoxaluria was induced by adding 0.75% ethylene glycol (EG) to the drinking water of male Wistar rats. After 7, 21, and 42 days of treatment, urinary biochemistry, oxalate levels, and lipid peroxides were measured. Kidney calculi were examined by polarizing microscopy. In the second part of the experiments, 1, 10, 20, and 30 mg kg,1 hr,1 oxalate was infused, by means of an intrarenal arterial catheter (IRA), into normal rats sequentially. Superoxide dismutase (SOD) infusion by means of IRA, in addition to oxalate, was also performed to check its influence on the altered renal function after oxalate infusion. In both the acute and chronic groups, renal blood flow (RBF), cortical microvascular blood flow (CMVBF), glomerular filtration rate (GFR), urine flow (UV), and urinary sodium excretion (UNaV) were measured, and chemiluminescence (CL) was examined in the renal venous blood. Results Levels of urinary lipid peroxides and enzymuria had increased since day 7, and increased the size of numbers of CaOx crystals in the kidney were noted beginning on day 21, but elevated CL was detectable only on day 7 after 0.75% EG treatment. Decreased UV and UNaV were noted in the 42-day EG group, although the 24-hr creatinine clearance values were normal in all experimental groups. On the other hand, RBF, GFR, and CMVBF were attenuated with elevated FR when the oxalate concentration was higher than 10 mg kg,1 hr,1 in the acute oxalate infusion group. With SOD pretreatment, the decreased RBF, GFR, and CMVBF could be reversed at 10 mg kg,1 hr,1 of oxalate, and be partially reversed at 20. FR also could be reduced significantly at 10 and 20 mg kg,1 hr,1 of oxalate. Conclusions Decreased urine flow and sodium excretion were the main renal functions affected by chronic hyperoxaluria. However, that only the 42-day EG group had a decreased tubular function cannot be fully explained by the persistent tubular enzymuria and increased lipid peroxides that began on day 7 after EG treatment. With acute oxalate infusion, the major insult to renal function was renal hemodynamics. Pretreated SOD could reverse the attenuated hemodynamics and reduce the elevated FR partly, which suggested that FR is responsible for oxalate toxicity. Neurourol. Urodynam. 22:176,182, 2003. © 2003 Wiley-Liss, Inc. [source]

Extracorporeal Support: Improves Donor Renal Graft Function After Cardiac Death

AMERICAN JOURNAL OF TRANSPLANTATION, Issue 6 2010
A. Rojas-Pena
Donors after cardiac death (DCD) could increase the organ pool. Data supports good long-term renal graft survival. However, DCDs are <10% of deceased donors in the United States, due to delayed graft function, and primary nonfunction. These complications are minimized by extracorporeal support after cardiac death (ECS-DCD). This study assesses immediate and acute renal function from different donor types. DCDs kidneys were recovered by conventional rapid recovery or by ECS, and transplanted into nephrectomized healthy swine. Warm ischemia of 10 and 30 min were evaluated. Swine living donors were controls (LVD). ECS-DCDs were treated with 90 min of perfusion until organ recovery. After procurement, kidneys were cold storage 4,6 h. Renal vascular resistance (RVR), urine output (UO), urine protein concentration (UrPr) and creatinine clearance (CrCl), were collected during 4 h posttransplantation. All grafts functioned with adequate renal blood flow for 4 h. RVR at 4 h posttransplant returned to baseline only in the LVD group (0.36 mmHg/mL/min ± 0.03). RVR was higher in all DCDs (0.66 mmHg/mL/min ± 0.13), without differences between them. UO was >50 mL/h in all DCDs, except in DCD-30 (6.8 mL/h ± 1.7). DCD-30 had lower CrCl (0.9 mL/min ± 0.2) and higher UrPr >200 mg/dL, compared to other DCDs >10 mL/min and <160 mg/dL, respectively. Normothermic ECS can resuscitate kidneys to transplantable status after 30 min of cardiac arrest/WI. [source]

RGS4 Controls Renal Blood Flow and Inhibits Cyclosporine-Mediated Nephrotoxicity

Connexin abundance in resistance vessels from the renal microcirculation in normo- and hypertensive rats

APMIS, Issue 4 2009
THOMAS HARTIG BRAUNSTEIN
The expression of connexins in renal arterioles is believed to have a profound impact on conducted responses, regulation of arteriolar tonus and renal blood flow. We have previously shown that in renal preglomerular arterioles, conducted vasomotor responses are 40% greater in spontaneously hypertensive rats (SHR) than in normotensive Sprague,Dawley (SD) rats. Because conducted vasomotor responses depend on the cell,cell communication mediated through gap junctions, we hypothesized that the increased magnitude of conducted vasomotor response in SHR is associated with an increased amount of connexins in renal arterioles. To test this hypothesis, the amount of connexin 37 (Cx37), Cx40 and Cx43 was assessed in renal arterioles from normo- and hypertensive rats using quantitative immunofluorescence laser confocal miscroscopy. To account for differences in genetic background, we included both normotensive Wistar,Kyoto (WKY) and SD rats in the study. In all three strains of rats, and for all three isoforms, the expression of connexins was predominantly confined to the endothelial cells. We found a significantly increased abundance (240 ± 17.6%, p<0.05) of Cx37 in arterioles from WKY compared with SD and SHR. This high abundance of Cx37 was not related to blood pressure because normotensive SD demonstrated a level of Cx37 similar to that of SHR. Additionally, we found no evidence for an increased abundance of Cx40 and Cx43 in renal arterioles of SHR when compared with normotensive counterparts. [source]

Role of Humoral Mediators in, and Influence of a Liposomal Formulation on, Acute Amphotericin B Nephrotoxicity

BASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 4 2001
Ramzi Sabra
Both direct effects of amphotericin B on contractile vascular cells, and indirect effects, due to humoural mediators, have been proposed. This study examines the role of nitric oxide, endothelin and angiotensin II in the acute nephrotoxic effects of amphotericin B in rats, and compares the antifungal and nephrotoxic effects of liposomal amphotericin B and amphotericin B-deoxycholate. Anaesthetized rats were given infusions of amphotericin B-deoxycholate in the presence or absence of N-nitro-L-arginine, PD 145065, a non-specific endothelin receptor antagonist, and L-158809, an angiotensin II type I receptor antagonist, or increasing doses of liposomal amphotericin B. Amphotericin B-deoxycholate (0.03 mg/kg/min intravenously) caused a significant 44% reduction in glomerular filtration rate and 65% maximal fall in renal blood flow. N-Nitro-L-arginine-treated rats had a lower renal blood flow and glomerular filtration rate at baseline, but sustained similar reduction of 53% and 75% in these parameters, respectively. PD145065 and L-158809 did not modify these effects either. Increasing doses of liposomal amphotericin B (from 0.01 up to 0.50 mg/kg/min.) induced no change in either glomerular filtration rate or renal blood flow. In vitro susceptibility tests revealed similar potency for liposomal amphotericin B and amphotericin B-deoxycholate in their fungistatic effects and slightly higher potency for amphotericin B-deoxycholate in their fungicidal effect. These results suggest that endogenous endothelin, angiotensin II or nitric oxide systems are not involved in the nephrotoxic effects of amphotericin B. The liposomal amphotericin B results suggest that amphotericin B nephrotoxicity is due to a direct interaction of amphotericin B with renal cells that is prevented by its encapsulation in liposomes. [source]

ACUTE PRESSURE,NATRIURESIS RELATIONSHIP FOLLOWING WITHDRAWAL OF CHRONIC NORADRENALINE INFUSION

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 9 2007
EI Boesen
SUMMARY 1Pathological changes to the kidney, such as vascular remodelling, have been found in several models of hypertension and may contribute to the maintenance of hypertension or confer susceptibility to redeveloping hypertension after the original prohypertensive stimulus is withdrawn. 2To investigate whether noradrenaline-induced hypertension induces persistent, functionally important changes to the kidney, the acute pressure,natriuresis relationship was characterized in anaesthetized rats under controlled neural and hormonal conditions following chronic (14 days) intravenous infusion of noradrenaline (48 µg/kg per h) or vehicle (0.04 mg/mL ascorbic acid and 0.156 mg/mL NaH2PO4·2H2O in 10 IU/mL heparinized saline). 3Conscious mean arterial pressure was significantly elevated by infusion of noradrenaline at 48 µg/kg per h (+10 ± 2 mmHg at Day 14; P < 0.01 vs vehicle group). The acute relationships between arterial pressure and renal blood flow, glomerular filtration rate, Na+ excretion and urine flow were not significantly different between the noradrenaline- and vehicle-infused rats immediately after termination of noradrenaline infusion. 4In summary, chronic intravenous noradrenaline infusion did not cause persistent changes in renal function, indicating that, in contrast with many models of hypertension, this model does not induce underlying prohypertensive changes to the kidney. [source]

RENAL OXYGEN DELIVERY: MATCHING DELIVERY TO METABOLIC DEMAND

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 10 2006
Paul M O'Connor
SUMMARY 1The kidneys are second only to the heart in terms of O2 consumption; however, relative to other organs, the kidneys receive a very high blood flow and oxygen extraction in the healthy kidney is low. Despite low arterial,venous O2 extraction, the kidneys are particularly susceptible to hypoxic injury and much interest surrounds the role of renal hypoxia in the development and progression of both acute and chronic renal disease. 2Numerous regulatory mechanisms have been identified that act to maintain renal parenchymal oxygenation within homeostatic limits in the in vivo kidney. However, the processes by which many of these mechanisms act to modulate renal oxygenation and the factors that influence these processes remain poorly understood. 3A number of such mechanisms specific to the kidney are reviewed herein, including the relationship between renal blood flow and O2 consumption, pre- and post-glomerular arterial,venous O2 shunting, tubulovascular cross-talk, the differential control of regional kidney blood flow and the tubuloglomerular feedback mechanism. 4The roles of these mechanisms in the control of renal oxygenation, as well as how dysfunction of these mechanisms may lead to renal hypoxia, are discussed. [source]

MECHANISMS MEDIATING PRESSURE NATRIURESIS: WHAT WE KNOW and WHAT WE NEED TO FIND OUT

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2005
Roger G Evans
SUMMARY 1.,It is well established that pressure natriuresis plays a key role in long-term blood pressure regulation, but our understanding of the mechanisms underlying this process is incomplete. 2.,Pressure natriuresis is chiefly mediated by inhibition of tubular sodium reabsorption, because both total renal blood flow and glomerular filtration rate are efficiently autoregulated. Inhibition of active sodium transport within both the proximal and distal tubules likely makes a contribution. Increased renal interstitial hydrostatic pressure (RIHP) likely inhibits sodium reabsorption by altering passive diffusion through paracellular pathways in ,leaky' tubular elements. 3.,Nitric oxide and products of cytochrome P450-dependent arachidonic acid metabolism are key signalling mechanisms in pressure natriuresis, although their precise roles remain to be determined. 4.,The key unresolved question is, how is increased renal artery pressure ,sensed' by the kidney? One proposal rests on the notion that blood flow in the renal medulla is poorly autoregulated, so that increased renal artery pressure leads to increased renal medullary blood flow (MBF), which, in turn, leads to increased RIHP. An alternative proposal is that the process of autoregulation of renal blood flow leads to increased shear stress in the preglomerular vasculature and, so, release of nitric oxide and perhaps products of cytochrome P450-dependent arachidonic acid metabolism, which, in turn, drive the cascade of events that inhibit sodium reabsorption. 5.,Central to the arguments underlying these opposing hypotheses is the extent to which MBF is autoregulated. This remains highly controversial, largely because of the limitations of presently available methods for measurement of MBF. [source]

DIFFERENTIAL NEURAL CONTROL OF GLOMERULAR ULTRAFILTRATION

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2004
Kate M Denton
Summary 1.,The renal nerves constrict the renal vasculature, causing decreases in renal blood flow (RBF) and glomerular filtration rate (GFR). Whether renal haemodynamics are influenced by changes in renal nerve activity within the physiological range is a matter of debate. 2.,We have identified two morphologically distinct populations of nerves within the kidney, which are differentially distributed to the renal afferent and efferent arterioles. Type I nerves almost exclusively innervate the afferent arteriole whereas type II nerves are distributed equally on the afferent and efferent arterioles. We have also demonstrated that type II nerves are immunoreactive for neuropeptide Y, whereas type I nerves are not. 3.,This led us to hypothesize that, in the kidney, distinct populations of nerves innervate specific effector tissues and that these nerves may be selectively activated, setting the basis for the differential neural control of GFR. In physiological studies, we demonstrated that differential changes in glomerular capillary pressure occurred in response to graded reflex activation of the renal nerves, compatible with our hypothesis. 4.,Thus, sympathetic outflow may be capable of selectively increasing or decreasing glomerular capillary pressure and, hence, GFR by differentially activating separate populations of renal nerves. This has important implications for our understanding of the neural control of body fluid balance in health and disease. [source]

Lipoxygenase and cyclo-oxygenase products in the control of regional kidney blood flow in rabbits

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 11 2003
Jeremy J Oliver
Summary 1.,The aim of the present study was to examine the roles of cyclo-oxygenase (COX)- and lipoxygenase (LOX)-dependent arachidonate signalling cascades in the control of regional kidney blood flow. 2.,In pentobarbitone-anaesthetized rabbits treated with NG -nitro- l -arginine and glyceryl trinitrate to ,clamp' nitric oxide, we determined the effects of ibuprofen (a COX inhibitor) and esculetin (a LOX inhibitor) on resting systemic and renal haemodynamics and responses to renal arterial infusions of vasoconstrictors. 3.,Ibuprofen increased mean arterial pressure (14 ± 5%) and reduced medullary laser Doppler flux (MLDF; 26 ± 6%) when administered with esculetin. A similar pattern of responses was observed when ibuprofen was given alone, although the reduction in MLDF was not statistically significant. Esculetin tended to increase renal blood flow (RBF; 16 ± 7%) and MLDF (28 ± 13%) when given alone, but not when combined with ibuprofen. 4.,After vehicle, renal arterial infusions of noradrenaline, angiotensin II and endothelin-1 reduced RBF and cortical laser Doppler flux (CLDF), but not MLDF. In contrast, renal arterial [Phe2,Ile3,Orn8]-vasopressin reduced MLDF but not RBF or CLDF. Ibuprofen alone did not significantly affect these responses. Esculetin, when given alone, but not when combined with ibuprofen, enhanced noradrenaline-induced renal vasoconstriction. In contrast, esculetin did not significantly affect responses to [Phe2,Ile3,Orn8]-vasopressin, angiotensin II or endothelin-1. 5.,We conclude that COX products contribute to the maintenance of arterial pressure and renal medullary perfusion under ,nitric oxide clamp' conditions, but not to renal haemodynamic responses to the vasoconstrictors we tested. Lipoxygenase products may blunt noradrenaline-induced vasoconstriction, but our observations may, instead, reflect LOX-independent effects of esculetin. [source]

Neural control of the renal vasculature in angiotensin II-induced hypertension

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 10 2002
Rohit Ramchandra
Summary 1.,Chronic administration of angiotensin (Ang) II causes an increase in blood pressure via a multitude of actions, including direct vasoconstriction, hypertrophy and increased sympathetic nerve activity. In the present study, we assessed whether the hypertension resulting from chronic AngII alters the ability of the renal vasculature to respond to sympathetic activity. 2.,Angiotensin II was administered for 7 weeks via an osmotic minipump at a dose of 50 ng/kg per min, i.v., to a group of six rabbits. Blood pressure, measured at 0, 1, 2 and 6 weeks after insertion of the pump, increased from 76 ± 2 to 104 ± 6 mmHg at the end of 6 weeks, without any significant change in heart rate. The blood pressure in the control group remained constant at 76 ± 2 mmHg. 3.,After 7 weeks, rabbits were anaesthetized and the renal nerves were stimulated at 0.5, 1, 1.5, 2, 3, 5 or 8 Hz for 3 min at their supramaximal voltage (5.5 ± 1.0 V in the normotensive group and 6.5 ± 1.5 V in the hypertensive group) while the renal blood flow (RBF) response was recorded. Under anaesthesia, there was no difference in mean arterial pressure between the normotensive and hypertensive animals (77 ± 2 and 80 ± 7 mmHg, respectively). The resting RBF under these conditions was not significantly different in the hypertensive group (30 ± 4 vs 26 ± 5 mL/min in the normotensive vs hypertensive group, respectively). 4.,Stimulation at increasing frequencies was associated with increasing reductions in RBF (e.g. 36 ± 8% at 2 Hz in normotensive rabbits and 48 ± 7% at 2 Hz in hypertensive rabbits). However, there were no significant differences between RBF responses in normotensive and hypertensive rabbits. 5.,We conclude that hypertension associated with chronic AngII administration does not alter the response in RBF to electrical stimulation of the nerves. [source]