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 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.

Renal medullary blood flow: its measurement and physiology

1986 ◽  
Vol 64 (7) ◽  
pp. 873-880 ◽  
Author(s):  
W. A. Cupples
Keyword(s):  
Blood Flow ◽  
Renal Medulla ◽  
Vascular Bundles ◽  
Medullary Blood Flow ◽  
Vasa Recta ◽  
Countercurrent Exchange ◽  
Renal Medullary Blood Flow ◽  
Urinary Concentrating Ability ◽  
Velocity Tracking ◽  
Uptake Method

The vasculature of the mammalian renal medulla is complex, having neither discrete input nor output. There is also efficient countercurrent exchange between ascending and descending vasa recta in the vascular bundles. These considerations have hampered measurement of medullary blood flow since they impose pronounced constraints on methods used to assess flow. Three main strategies have been used: (i) indicator extraction; (ii) erythrocyte velocity tracking; and (iii) indicator dilution. These are discussed with respect to their assumptions, requirements, and limitations. There is a consensus that medullary blood flow is autoregulated, albeit over a narrower pressure range than is total renal blood flow. When normalized to gram tissue weight, medullary blood flow in the dog is similar to that in the rat, on the order of 1 to 1.5 mL∙min−1∙g−1. This is considerably greater than estimated by the radioiodinated albumin uptake method which has severe conceptual and practical problems. From both theoretical and experimental evidence it ssems that urinary concentrating ability is considerably less sensitive to changes in medullary blood flow than is often assumed.

scholarly journals Autoregulation of renal medullary blood flow in rabbits

2003 ◽  
Vol 284 (1) ◽  
pp. R233-R244 ◽  
Author(s):  
Gabriela A. Eppel ◽  
Göran Bergström ◽  
Warwick P. Anderson ◽  
Roger G. Evans
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Laser Doppler Flowmetry ◽  
Systemic Arterial Pressure ◽  
Laser Doppler ◽  
Kidney Volume ◽  
Doppler Flowmetry ◽  
Medullary Blood Flow ◽  
Vasa Recta ◽  
Renal Medullary Blood Flow

We examined the extent of renal medullary blood flow (MBF) autoregulation in pentobarbital-anesthetized rabbits. Two methods for altering renal arterial pressure (RAP) were compared: the conventional method of graded suprarenal aortic occlusion and an extracorporeal circuit that allows RAP to be increased above systemic arterial pressure. Changes in MBF were estimated by laser-Doppler flowmetry, which appears to predominantly reflect erythrocyte velocity, rather than flow, in the kidney. We compared responses using a dual-fiber needle probe held in place by a micromanipulator, with responses from a single-fiber probe anchored to the renal capsule, to test whether RAP-induced changes in kidney volume confound medullary laser-Doppler flux (MLDF) measurements. MLDF responses were similar for both probe types and both methods for altering RAP. MLDF changed little as RAP was altered from 50 to ≥170 mmHg (24 ± 22% change). Within the same RAP range, RBF increased by 296 ± 48%. Urine flow and sodium excretion also increased with increasing RAP. Thus pressure diuresis/natriuresis proceeds in the absence of measurable increases in medullary erythrocyte velocity estimated by laser-Doppler flowmetry. These data do not, however, exclude the possibility that MBF is increased with increasing RAP in this model, because vasa recta recruitment may occur.

Abstract P166: The Effects of V2 Receptor Antagonist Treatment on the Renal Medullary Circulation and Urinary Sodium Excretion in Rat

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Yusuke Ohsaki ◽  
Takefumi Mori ◽  
Kento Akao ◽  
Yoshimi Nakamichi ◽  
Chika Takahashi ◽  
...  
Keyword(s):  
Blood Flow ◽  
Urine Volume ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Sodium Reabsorption ◽  
No Production ◽  
Doppler Flowmetry ◽  
Medullary Blood Flow ◽  
V2 Receptor ◽  
Renal Medullary Blood Flow

Objective: V2 receptor (V2R) antagonist increases aquaresis, and was reported to have renoprotective and natriuretic effect, although the mechanism is not fully clarified. Renal medullary hemodynamics contributes sodium retention and renal injury. Therefore, the present study was designed to evaluate the effect of V2R antagonist on renal medullary blood flow. Methods: Catheter was inserted in femoral artery and vein of anesthetized SD rats to monitor blood pressure (BP), heart rate (HR) and to infuse drugs, respectively. Renal medullary blood flow (MBF) and renal medullary oxygen pressure (pO2) were measured with laser-Doppler flowmetry or oxygen microelectrode, respectively. V2R antagonist, OPC-31260 (OPC, 0.25mg/kg bw/h) or furosemide (Furo, 0.5mg/kg bw/h) was intravenously administrated for 90min. Urine was collected in 30 min interval and urinary sodium (UNaV), hydrogen peroxide (UH2O2V) and [nitrate + nitrite] (UNOxV) excretion were measured. Results: OPC and Furo treatment did not change BP and HR. Urine volume was significantly increased by OPC (1.1+0.2 to 6.1+0.5 g/30 min) and Furo (1.4+0.6 to 4.7+0.3 g/30 min) treatment but was not different between groups. MBF was significantly decreased in Furo (12+4% decrease from baseline), while OPC did not changed MBF (1+3% increase from baseline). pO2 was significantly increased by both OPC and Furo treatment (20+6 and 27+10% increase from baseline, respectively). UNaV was significantly increased in OPC (0.10+0.02 to 0.44+0.05 mEq/30 min) and Furo (0.14+0.08 to 0.69+0.06 mEq/30 min) treatment, the increase of UNaV was significantly higher in Furo than OPC group. UH2O2V was significantly increased by Furo treatment (16+4 to 28+6 nmol/30 min), while did not change in OPC treatment (10+2 to 19+4 nmol/30 min). UNOx was significantly increased in OPC treatment (211+30 to 376+45 nmol/30 min), while did not change in Furo treatment (142+27 to 237+75 nmol/30 min). Conclusion: OPC treatment increased NO production. Increased NO could contribute to decrease of sodium reabsorption, result in increase of renal medullary pO2. This scheme could be one on the mechanisms of renal protective effect by V2R antagonist treatment.

Relationship between renal perfusion pressure and blood flow in different regions of the kidney

1993 ◽  
Vol 264 (3) ◽  
pp. R578-R583 ◽  
Author(s):  
D. L. Mattson ◽  
S. Lu ◽  
R. J. Roman ◽  
A. W. Cowley
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Laser Doppler Flowmetry ◽  
Renal Cortex ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Doppler Flowmetry ◽  
Cortical Blood Flow ◽  
Renal Perfusion Pressure ◽  
Medullary Blood Flow

The present study examined the autoregulation of blood flow in different regions of the renal cortex and medulla in volume-expanded or hydropenic anesthetized rats. Blood flow was measured in the whole kidney by electromagnetic flowmetry, in the superficial cortex with implanted fibers and external probes for laser-Doppler flowmetry, and in the deep cortex and inner and outer medulla with implanted fibers for laser-Doppler flowmetry. At renal perfusion pressure > 100 mmHg, renal blood flow, superficial cortical blood flow, and deep cortical blood flow were all very well autoregulated in both volume-expanded and hydropenic rats. Inner and outer medullary blood flow were also well autoregulated in hydropenia, but blood flow in these regions was very poorly autoregulated in volume-expanded animals. As renal perfusion pressure was decreased below 100 mmHg in volume-expanded and hydropenic animals, renal blood flow, superficial and deep cortical blood flow, and inner and outer medullary blood flow all decreased. The results of these experiments demonstrate that blood flow in both the inner and outer portions of the renal medulla of the kidney is poorly autoregulated in volume-expanded rats but well autoregulated in hydropenic animals. In contrast, blood flow in all regions of the renal cortex is well autoregulated in both volume-expanded and hydropenic animals. These results suggest that changes in resistance in the postglomerular circulation of deep nephrons are responsible for the poor autoregulation of medullary blood flow in volume expansion despite well autoregulated cortical blood flow.

Renal medullary tissue oxygenation is dependent on both cortical and medullary blood flow

2006 ◽  
Vol 290 (3) ◽  
pp. F688-F694 ◽  
Author(s):  
Paul M. O'Connor ◽  
Michelle M. Kett ◽  
Warwick P. Anderson ◽  
Roger G. Evans
Keyword(s):  
Blood Flow ◽  
Tissue Oxygenation ◽  
Renal Perfusion ◽  
Renal Nerves ◽  
Sodium Reabsorption ◽  
Ang Ii ◽  
Medullary Blood Flow ◽  
Medullary Tissue ◽  
Cortical Ischemia ◽  
Cortical Perfusion

The aim of the current study was to determine whether renal medullary oxygenation is independent of the level of cortical blood flow by testing responses to stimuli that selectively reduce blood flow in either the cortex or medulla. In anesthetized rabbits, renal arterial infusion of [Phe2,Ile3,Orn8]-vasopressin selectively reduced medullary perfusion and Po2 (−54 ± 24 and −50 ± 10%, respectively) but did not significantly affect cortical perfusion or tissue oxygenation. In contrast, stimulation of the renal nerves resulted in renal cortical ischemia with reductions in total renal blood flow (−76 ± 3% at 4 Hz), cortical perfusion (−57 ± 17%), and cortical Po2 (−44 ± 12%). Medullary tissue Po2 was reduced by −70 ± 5% at 4 Hz, despite medullary perfusion being unaffected and distal tubular sodium reabsorption being reduced (by −83.3 ± 1.2% from baseline). In anesthetized rats, in which renal perfusion pressure was maintained with an aortic constrictor, intravenous infusion of ANG II (0.5–5 μg·kg−1·min−1) dose dependently reduced cortical perfusion (up to −65 ± 3%; P < 0.001) and cortical Po2 (up to −57 ± 4%; P < 0.05). However, medullary perfusion was only significantly reduced at the highest dose (5 μg·kg−1·min−1; by 29 ± 6%). Medullary perfusion was not reduced by 1 μg·kg−1·min−1 ANG II, but medullary Po2 was significantly reduced (−12 ± 4%). Thus, although cortical and medullary blood flow may be independently regulated, medullary oxygenation may be compromised during moderate to severe cortical ischemia even when medullary blood flow is maintained.

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.

Restoration of vasa recta hemodynamics and pressure natriuresis in SHR by L-arginine

1995 ◽  
Vol 268 (5) ◽  
pp. F907-F912 ◽  
Author(s):  
T. S. Larson ◽  
J. C. Lockhart
Keyword(s):  
Blood Flow ◽  
Perfusion Pressure ◽  
Spontaneously Hypertensive Rat ◽  
Urinary Sodium Excretion ◽  
Renal Perfusion ◽  
Spontaneously Hypertensive ◽  
Medullary Blood Flow ◽  
Vasa Recta ◽  
Wistar Kyoto ◽  
Pressure Natriuresis

An increase in medullary blood flow has been implicated as a mediator of the natriuresis following increases in renal perfusion pressure (RPP). We examined whether administration of L-arginine, the substrate for nitric oxide production, restores the impaired vasa recta hemodynamic response to increases in RPP and the blunted pressure natriuresis of the spontaneously hypertensive rat (SHR). The response of descending (QDVR) and ascending vasa recta blood flow (QAVR) and of urinary sodium excretion (UNaV) was examined as RPP was increased by means of an adjustable aortic clamp placed above the renal arteries in young SHR and Wistar-Kyoto (WKY) rats. When RPP was increased in SHR receiving infusion of L-arginine (n = 7), QDVR and QAVR increased significantly in association with increases in UNaV. In SHR receiving the inactive enantiomer, D-arginine (n = 7), similar increases in RPP failed to increase QAVR and QDVR and were associated with an attenuated increase in UNaV. WKY animals infused with either D-arginine or L-arginine had increases in QDVR, QAVR, and UNaV in response to increases in RPP that were of similar magnitude to SHR receiving L-arginine. Thus the administration of L-arginine to SHR restores the pressure-dependent increases in renal medullary hemodynamics in association with restoration of pressure natriuresis.

Angiotensin II and prostaglandins in control of vasa recta blood flow

1988 ◽  
Vol 254 (3) ◽  
pp. F417-F424 ◽  
Author(s):  
W. A. Cupples ◽  
T. Sakai ◽  
D. J. Marsh
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Renal Medulla ◽  
Medullary Blood Flow ◽  
Vasa Recta ◽  
Electromagnetic Flow Probe ◽  
Angiotensin Blockade

Angiotensin II has been implicated in the regulation of medullary blood flow and is known to interact with prostaglandins at sites within the kidney. Therefore the role of angiotensin in control of vasa recta blood flow was studied in antidiuretic, Munich-Wistar rats. We also tested the hypothesis that prostaglandins act to modulate the effect of angiotensin. Total renal blood flow was measured by an electromagnetic flow probe, vasa recta blood flow by a dual-slit method. Captopril was used to confirm that angiotensin blockade increased renal blood flow (by 15 +/- 4%). Captopril and saralasin were used to show that angiotensin blockade increased vasa recta blood flow (by 23 +/- 9 and 14 +/- 7%, respectively). The results demonstrate a tonic constrictor effect of angiotensin in the renal medulla. Exogenous angiotensin II, delivered intravenously, failed to mimic the effect of endogenous angiotensin. Indomethacin did not alter blood pressure or renal blood flow but did reduce vasa recta blood flow by 20 +/- 3%, suggesting that prostaglandins act preferentially on the medullary circulation. Nor did it alter the response of blood pressure, of renal blood flow, or of vasa recta blood flow to captopril. Moreover, prior angiotensin blockade with either captopril or saralasin enhanced the medullary vasoconstrictor effect of indomethacin (P less than 0.05). These results are not consistent with the hypothesis that prostaglandins act primarily as angiotensin modulators. They suggest that the medullary interaction between angiotensin and prostaglandins differs from that in the cortex.

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