Renal cortical and medullary blood flow responses during water restriction: role of vasopressin

1996 ◽  
Vol 270 (6) ◽  
pp. R1257-R1264 ◽  
Author(s):  
K. G. Franchini ◽  
A. W. Cowley
Keyword(s):  
Blood Flow ◽  
Urine Osmolality ◽  
Control Group ◽  
Water Restriction ◽  
Vascular Effect ◽  
Doppler Flowmetry ◽  
Medullary Blood Flow ◽  
Urinary Concentrating Ability ◽  
Interstitial Infusion

Experiments were performed in unanesthetized rats to determine responses to 48 h water restriction of the renal regional microcirculation (cortex, outer medulla, and inner medulla) using implanted optical fibers and laser-Doppler flowmetry. The role of vasopressin (AVP) as a mediator of renal regional blood low changes and its contribution to urinary concentrating ability were assessed by continuous intramedullary interstitial infusion of specific V1 receptor antagonist d(CH2)5 [Tyr-(Me)2, Ala-NH2]AVP (2ng . kg-1 . min-1). Inner medullary blood flow decreased 34% at the end of 48 h of water restriction, whereas cortical and outer medullary flow did not change. This fall in inner medullary blood flow was substantially attenuated (18%) by the continuous interstitial infusion of the antagonist. Plasma AVP levels increased from control levels of 3.4 +/- 1.1 to 20.5 +/- 5.4 pg/ml (P < 0.05) by the end of the 48-h period of water restriction. Arterial pressure increased slightly but significantly during water restriction in the control rats. Infusion of antagonist impaired the maximal urinary concentrating ability, as demonstrated by the lower urine osmolality in this group than in the control group (1,893 +/- 49 vs. 2,419 +/- 225 mosmol/kg H2O; P < 0.05) measured during the second day of water restriction. Sodium and urea concentration decreased 20 and 22%, respectively, indicating that both contributed to the lower urine osmolality observed in the group of rats receiving the antagonist. We conclude that water restriction induces a selective decrease in inner medullary blood flow, which is mediated almost completely by endogenously released AVP. This vascular effect of AVP contributes to the maximum concentrating ability of the kidney.

Role of renal medullary adenosine in the control of blood flow and sodium excretion

1999 ◽  
Vol 276 (3) ◽  
pp. R790-R798 ◽  
Author(s):  
Ai-Ping Zou ◽  
Kasem Nithipatikom ◽  
Pin-Lan Li ◽  
Allen W. Cowley
Keyword(s):  
Blood Flow ◽  
Sodium Excretion ◽  
Renal Medulla ◽  
Urine Flow ◽  
Doppler Flowmetry ◽  
Blood Flows ◽  
Medullary Blood Flow ◽  
Adenosine Concentration ◽  
Interstitial Infusion

This study determined the levels of adenosine in the renal medullary interstitium using microdialysis and fluorescence HPLC techniques and examined the role of endogenous adenosine in the control of medullary blood flow and sodium excretion by infusing the specific adenosine receptor antagonists or agonists into the renal medulla of anesthetized Sprague-Dawley rats. Renal cortical and medullary blood flows were measured using laser-Doppler flowmetry. Analysis of microdialyzed samples showed that the adenosine concentration in the renal medullary interstitial dialysate averaged 212 ± 5.2 nM, which was significantly higher than 55.6 ± 5.3 nM in the renal cortex ( n = 9). Renal medullary interstitial infusion of a selective A1antagonist, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX; 300 pmol ⋅ kg−1 ⋅ min−1, n = 8), did not alter renal blood flows, but increased urine flow by 37% and sodium excretion by 42%. In contrast, renal medullary infusion of the selective A2 receptor blocker 3,7-dimethyl-1-propargylxanthine (DMPX; 150 pmol ⋅ kg−1 ⋅ min−1, n = 9) decreased outer medullary blood flow (OMBF) by 28%, inner medullary blood flows (IMBF) by 21%, and sodium excretion by 35%. Renal medullary interstitial infusion of adenosine produced a dose-dependent increase in OMBF, IMBF, urine flow, and sodium excretion at doses from 3 to 300 pmol ⋅ kg−1 ⋅ min−1( n = 7). These effects of adenosine were markedly attenuated by the pretreatment of DMPX, but unaltered by DPCPX. Infusion of a selective A3receptor agonist, N 6-benzyl-5′-( N-ethylcarbonxamido)adenosine (300 pmol ⋅ kg−1 ⋅ min−1, n = 6) into the renal medulla had no effect on medullary blood flows or renal function. Glomerular filtration rate and arterial pressure were not changed by medullary infusion of any drugs. Our results indicate that endogenous medullary adenosine at physiological concentrations serves to dilate medullary vessels via A2 receptors, resulting in a natriuretic response that overrides the tubular A1 receptor-mediated antinatriuretic effects.

Influence of the renal medullary circulation on the control of sodium excretion

1993 ◽  
Vol 265 (5) ◽  
pp. R963-R973 ◽  
Author(s):  
R. J. Roman ◽  
A. P. Zou
Keyword(s):  
Blood Flow ◽  
Renal Perfusion ◽  
Sodium Reabsorption ◽  
Doppler Flowmetry ◽  
Medullary Blood Flow ◽  
Tubular Sodium Reabsorption ◽  
Vasa Recta ◽  
Urinary Concentrating Ability ◽  
Reliable Methods

Although the role of the renal medullary circulation in the control of urinary concentrating ability is well established, its potential influence on tubular sodium reabsorption is not generally recognized. Nearly 30 years ago, changes in the intrarenal distribution of blood flow were first proposed to contribute to the natriuretic response to volume expansion. However, the lack of reliable methods for studying medullary blood flow limited progress in this area. The recent development of laser-Doppler flowmetry and videomicroscopic techniques for the study of the vasa recta circulation has renewed interest in the role of medullary hemodynamics in the control of sodium reabsorption. Results of these studies indicate that changes in renal medullary hemodynamics alter renal interstitial pressure and the medullary solute gradient and play an important role in the natriuretic response to elevations in renal perfusion pressure, intravenous infusion of saline, and changes in tubular sodium reabsorption produced by vasoactive compounds. What is emerging from these studies is the view that changes in renal medullary hemodynamics represent an important but misunderstood and long-ignored factor in the control of tubular sodium reabsorption.

Renal medullary interstitial infusion of diltiazem alters sodium and water excretion in rats

1992 ◽  
Vol 263 (5) ◽  
pp. R1064-R1070 ◽  
Author(s):  
S. Lu ◽  
R. J. Roman ◽  
D. L. Mattson ◽  
A. W. Cowley
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Urine Flow ◽  
Water Excretion ◽  
Doppler Flowmetry ◽  
Blood Flows ◽  
Electromagnetic Flow Probe ◽  
Interstitial Infusion

The role of renal papillary blood flow in regulation of fluid and electrolyte excretion was examined. The effects of an acute infusion of diltiazem (5 micrograms.kg-1 x min-1) into the renal medullary interstitium on papillary blood flow and sodium and water excretion were studied. Changes of renal blood flow were measured using an electromagnetic flow probe. Cortical and papillary blood flows were measured using laser-Doppler flowmetry. Renal and cortical blood flows were unchanged during medullary interstitial infusion of diltiazem, but papillary blood flow increased 26% (P < 0.05) and remained elevated for 1 h after diltiazem infusion was discontinued. Glomerular filtration rate (GFR) of the infused kidney increased by 21% from a control of 1.0 +/- 0.1 ml.min-1 x g-1 during infusion of diltiazem (P < 0.05), but it returned to control after diltiazem infusion was stopped. Urine flow and sodium excretion increased by 70% (P < 0.05), and fractional sodium excretion rose from 1.5 +/- 0.2 to 2.4 +/- 0.3% of the filtered load during the hour after diltiazem infusion. Renal blood flow, cortical and papillary blood flow, GFR, urine flow, and sodium excretion in the 0.9% sodium chloride vehicle-infused kidney were not significantly altered during the experiment. Intravenous infusion of the same dose of diltiazem (5 micrograms.kg-1 x min-1) increased GFR by 22%, but had no effect on urine flow and sodium excretion. These results indicate that renal medullary interstitial infusion of diltiazem selectively increased renal papillary blood flow, which was associated with an increase of sodium and water excretion.

Sensitivity of the renal medullary circulation to plasma vasopressin

1996 ◽  
Vol 271 (3) ◽  
pp. R647-R653 ◽  
Author(s):  
K. G. Franchini ◽  
A. W. Cowley
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Intravenous Infusion ◽  
Control Level ◽  
Flow Distribution ◽  
Renal Medulla ◽  
Urine Osmolality ◽  
Water Restriction ◽  
Doppler Flowmetry ◽  
Total Renal Blood Flow

Studies were carried out to determine the effects of physiological changes of plasma arginine vasopressin (AVP) on blood flow distribution in the renal cortex and medulla. Acute decerebration was performed so that studies could be carried out within the low physiological range of circulating AVP. Changes of renal cortical and medullary microcirculatory blood flow were measured with implanted optical fibers and laser-Doppler flowmetry, and total renal blood flow was measured with transit-time ultrasonography. During intravenous infusion of increasing doses of AVP, when plasma AVP was increased in steps from 2.9 to 11.2 pg/ml by intravenous infusion, mean arterial pressure (98 +/- 3 mmHg), total renal blood flow (8.2 +/- 0.6 ml. min-1.g kidney-1), and blood flow in the microcirculation of the cortex (2.11 +/- 0.28 V) remained unchanged, whereas that in the renal medulla decreased progressively. Medullary flow was significantly reduced when circulating levels of AVP increased from a control level of 2.8 to 5.0 pg/ml. The reductions of medullary flow were accompanied by parallel increases of urine osmolality. These data indicate that the vessels supplying the renal medullary circulation are sensitive within the range of plasma AVP concentrations observed with moderate water restriction. The medullary circulation exhibits a sensitivity AVP that parallels that found in the medullary collecting ducts.

Regulation of intrarenal blood flow in experimental heart failure: role of endothelin and nitric oxide

1998 ◽  
Vol 274 (4) ◽  
pp. F766-F774 ◽  
Author(s):  
Zaid Abassi ◽  
Konstantin Gurbanov ◽  
Irith Rubinstein ◽  
Ori S. Better ◽  
Aaron Hoffman ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Blood Flow ◽  
Doppler Flowmetry ◽  
Medullary Blood Flow ◽  
The Face ◽  
Enos Mrna ◽  
Intrarenal Blood Flow ◽  
Altered Regulation

Congestive heart failure (CHF) is associated with a marked decrease in cortical blood flow and preservation of medullary blood flow. In the present study we tested the hypothesis that changes in the endothelin (ET) and nitric oxide (NO) systems in the kidney may contribute to the altered intrarenal hemodynamics in rats with aortocaval fistula, an experimental model of CHF. Cortical and medullary blood flow were measured simultaneously by laser-Doppler flowmetry in controls and rats with compensated and decompensated CHF. As previously reported [K. Gurbanov, I. Rubinstein, A. Hoffman, Z. Abassi, O. S. Better, and J. Winaver. Am. J. Physiol. 271 ( Renal Fluid Electrolyte Physiol. 40): F1166–F1172, 1996], administration of ET-1 in control rats produced a sustained cortical vasoconstriction and a transient medullary vasodilatory response. In rats with decompensated CHF, cortical vasoconstriction was severely blunted, whereas ET-1-induced medullary vasodilation was significantly prolonged. This prolonged response was mimicked by IRL-1620, a specific ETB agonist, and partially abolished by NO synthase (NOS) blockade. In line with these findings, expression of ET-1, ETA and ETB receptors, and endothelial NOS (eNOS), assessed by RT-PCR, and eNOS immunoreactivity, assessed by Western blotting, was significantly higher in the medulla than in the cortex. Moreover, expression of ET-1 mRNA in the cortex and eNOS mRNA in the cortex and the medulla increased in proportion to the severity of heart failure. These findings indicate that CHF is associated with altered regulation of intrarenal blood flow, which reflects alterations in expression and activity of the ET and NO systems. It is further suggested that exaggerated NO activity in the medulla contributes to preservation of medullary blood flow in the face of cortical vasoconstriction in CHF.

Control of renal medullary blood flow by vasopressin V1 and V2 receptors

1995 ◽  
Vol 269 (1) ◽  
pp. R193-R200 ◽  
Author(s):  
K. Nakanishi ◽  
D. L. Mattson ◽  
V. Gross ◽  
R. J. Roman ◽  
A. W. Cowley
Keyword(s):  
Blood Flow ◽  
Laser Doppler Flowmetry ◽  
Arginine Vasopressin ◽  
Laser Doppler ◽  
Receptor Stimulation ◽  
Doppler Flowmetry ◽  
Medullary Blood Flow ◽  
V2 Receptor ◽  
Renal Medullary Blood Flow ◽  
Interstitial Infusion

Experiments were performed in anesthetized renal-denervated rats to determine the contribution of renal medullary vasopressin V1 and V2 receptor stimulation in the regulation of renal medullary blood flow. Renal medullary interstitial infusion of the selective V1 agonist [Phe2,Ile3,Orn8]vasopressin (2 ng.kg-1.min-1) significantly decreased outer medullary blood flow by 15% and inner medullary blood flow by 35%, as measured with implanted optical fibers for laser-Doppler flowmetry. Medullary interstitial infusion of equimolar doses of arginine vasopressin (AVP) also decreased outer medullary blood flow by 15% but decreased inner medullary blood flow by only 17%, a decrease significantly less than that during the infusion of the V1 agonist. These results were confirmed in videomicroscopy experiments on the exposed papilla, which demonstrated that the V1 agonist and AVP decreased descending and ascending vasa recta capillary red blood cell velocity and calculated blood flow, with greater decreases during infusion of the V1 agonist. In further laser-Doppler flowmetry studies, stimulation of V2 receptors by medullary interstitial infusion of 1-desamino-8-D-arginine vasopressin (2 ng.kg-1.min-1) or AVP in rats pretreated with the vasopressin V1 receptor antagonist d(CH2)5[Tyr(Me)2,Ala-NH2]AVP increased renal medullary blood flow by 16 +/- 3 and 27 +/- 8%, respectively. The present experiments indicate that vasopressin V1 receptor stimulation serves to decrease renal medullary blood flow while V2 receptor stimulation appears to increase renal medullary blood flow; however, the net effect of AVP is to decrease renal medullary blood flow.

Vasopressin modulation of medullary blood flow and pressure-natriuresis-diuresis in the decerebrated rat

1997 ◽  
Vol 272 (5) ◽  
pp. R1472-R1479 ◽  
Author(s):  
K. G. Franchini ◽  
D. L. Mattson ◽  
A. W. Cowley
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Fluid Pressure ◽  
Renal Medulla ◽  
Urinary Sodium Excretion ◽  
Water Restriction ◽  
Vascular Effects ◽  
Doppler Flowmetry ◽  
Physiological Importance ◽  
Medullary Blood Flow

Studies in our laboratory and others have demonstrated that arginine vasopressin (AVP) exerts potent vasoconstrictor actions on the vessels supplying the renal medulla. The physiological importance of these vascular effects of AVP has been difficult to assess because of high endogenous levels of AVP in anesthetized, surgically prepared animals. We have developed a decerebrated, hypophysectomized, renal-denervated rat model that enables us to study the effects of low levels of AVP on the pressure-diuresis, relationship under acute conditions. These rats maintain normal mean arterial pressure (MAP) and plasma AVP (2.5 pg/ml). Cortical and medullary blood flow (CBF and MBF, respectively) were measured by laser-Doppler flowmetry and total renal blood flow (RBF) by transit time flowmetry. Renal interstitial fluid pressure (RIFP) and urinary sodium excretion (UNaV) responses were determined during controlled increases of MAP produced by aortic occlusion below the renal arteries. From a baseline of 97 +/- 2 mmHg, 30% increases in MAP resulted in a 63% increase in MBF, 35% increase in RIFP, and sixfold increase in UNaV, whereas CBF and RBF remained unchanged. Infusion of AVP (0.50 ng.kg-1.min-1, which increased plasma AVP from normal control levels of 3 pg/ml to 11 pg/ml) produced no change in baseline MAP, RBF, or CBF but lowered MBF by 24%, RIFP by 26%, and UNaV by 71%. The slope of the relationship of AP and UNaV, MBF, and RIP was reduced to nearly zero by these small increases of plasma AVP. We conclude that an increase of plasma AVP in the range that occurs with water restriction decreases MBF selectively and greatly attenuates the arterial pressure-MBF and pressure-natriuretic relationship.

scholarly journals The Role of Neuronal Nitric Oxide Synthase in Regulation of Cerebral Blood Flow in Normocapnia and Hypercapnia in Rats

1995 ◽  
Vol 15 (5) ◽  
pp. 774-778 ◽  
Author(s):  
Qiong Wang ◽  
Dale A. Pelligrino ◽  
Verna L. Baughman ◽  
Heidi M. Koenig ◽  
Ronald F. Albrecht
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Nitric Oxide Synthase ◽  
Inhibitory Action ◽  
Neuronal Nitric Oxide Synthase ◽  
Muscarinic Agonist ◽  
Doppler Flowmetry ◽  
Nos Inhibitors ◽  
Oxide Synthase

The nitric oxide synthase (NOS) inhibitors, nitro-L-arginine, its methyl ester, and N-monomethyl-L-arginine, have been shown to attenuate resting CBF and hypercapnia-induced cerebrovasodilation. Those agents nonspecifically inhibit the endothelial and neuronal NOS (eNOS and nNOS). In the present study, we used a novel nNOS inhibitor, 7-nitroindazole (7-NI) to examine the role of nNOS in CBF during normocapnia and hypercapnia in fentanyl/N2O-anesthetized rats. CBF was monitored using laser-Doppler flowmetry. Administration of 7-NI (80 mg kg−1 i.p.) reduced cortical brain NOS activity by 57%, the resting CBF by 19–27%, and the CBF response to hypercapnia by 60%. The 60% reduction was similar in magnitude to the CBF reductions observed in previous studies in which nonspecific NOS inhibitors were used. In the present study, 7-NI did not increase the MABP. Furthermore, the CBF response to oxotremorine, a blood–brain barrier permeant muscarinic agonist that induces cerebrovasodilation via endothelium-derived NO, was unaffected by 7-NI. These results confirmed that 7-NI does not influence eNOS; they also indicated that the effects of 7-NI on the resting CBF and on the CBF response to hypercapnia in this study were solely related to its inhibitory action on nNOS. The results further suggest that the NO synthesized by the action of nNOS participates in regulation of basal CBF and is the major, if not the only, category of NO contributing to the hypercapnic CBF response.

Splanchnic blood flow and hepatic glucose production in exercising humans: role of renin-angiotensin system

2001 ◽  
Vol 281 (6) ◽  
pp. R1854-R1861 ◽  
Author(s):  
Raynald Bergeron ◽  
Michael Kjær ◽  
Lene Simonsen ◽  
Jens Bülow ◽  
Dorthe Skovgaard ◽  
...  
Keyword(s):  
Blood Flow ◽  
Renin Angiotensin System ◽  
Glucose Production ◽  
Splanchnic Blood Flow ◽  
Control Group ◽  
Moderate Exercise ◽  
Ang Ii ◽  
Angiotensin System ◽  
Renin Angiotensin

The study examined the implication of the renin-angiotensin system (RAS) in regulation of splanchnic blood flow and glucose production in exercising humans. Subjects cycled for 40 min at 50% maximal O2 consumption (V˙o 2 max) followed by 30 min at 70% V˙o 2 maxeither with [angiotensin-converting enzyme (ACE) blockade] or without (control) administration of the ACE inhibitor enalapril (10 mg iv). Splanchnic blood flow was estimated by indocyanine green, and splanchnic substrate exchange was determined by the arteriohepatic venous difference. Exercise led to an ∼20-fold increase ( P < 0.001) in ANG II levels in the control group (5.4 ± 1.0 to 102.0 ± 25.1 pg/ml), whereas this response was blunted during ACE blockade (8.1 ± 1.2 to 13.2 ± 2.4 pg/ml) and in response to an orthostatic challenge performed postexercise. Apart from lactate and cortisol, which were higher in the ACE-blockade group vs. the control group, hormones, metabolites, V˙o 2, and RER followed the same pattern of changes in ACE-blockade and control groups during exercise. Splanchnic blood flow (at rest: 1.67 ± 0.12, ACE blockade; 1.59 ± 0.18 l/min, control) decreased during moderate exercise (0.78 ± 0.07, ACE blockade; 0.74 ± 0.14 l/min, control), whereas splanchnic glucose production (at rest: 0.50 ± 0.06, ACE blockade; 0.68 ± 0.10 mmol/min, control) increased during moderate exercise (1.97 ± 0.29, ACE blockade; 1.91 ± 0.41 mmol/min, control). Refuting a major role of the RAS for these responses, no differences in the pattern of change of splanchnic blood flow and splanchnic glucose production were observed during ACE blockade compared with controls. This study demonstrates that the normal increase in ANG II levels observed during prolonged exercise in humans does not play a major role in the regulation of splanchnic blood flow and glucose production.

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