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.

Effect of acute renal decapsulation on pressure natriuresis in SHR and WKY rats

1989 ◽  
Vol 257 (5) ◽  
pp. F785-F789 ◽  
Author(s):  
A. A. Khraibi ◽  
F. G. Knox
Keyword(s):  
Spontaneously Hypertensive Rat ◽  
Fractional Excretion ◽  
Renal Perfusion ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Fractional Excretion Of Sodium ◽  
Diuretic Response ◽  
Wistar Kyoto ◽  
Pressure Natriuresis ◽  
Shr And Wky Rats

The objective of these experiments was to study pressure natriuresis in the Wistar-Kyoto (WKY) and the spontaneously hypertensive rat (SHR) during acute bilateral renal decapsulation, a maneuver that partially blocks the increase in renal interstitial hydrostatic pressure (RIHP). In control WKY rats (n = 7), at renal perfusion pressure (RPP) of 105 +/- 0.7 and 125 +/- 1.1 mmHg, RIHP increased from 4.4 +/- 0.4 to 7.2 +/- 0.7 mmHg (P less than 0.05) and fractional excretion of sodium (FENa) increased from 0.23 +/- 0.05 to 1.32 +/- 0.14% (P less than 0.05). Acute bilateral renal decapsulation (n = 6) blunted the increase in RIHP observed when RPP was increased in control WKY rats and abolished the pressure natriuretic and diuretic response. When RPP was allowed to increase from 106 +/- 0.8 to 130 +/- 2.2 mmHg in the WKY rats with decapsulated kidneys, RIHP increased from 3.8 +/- 0.5 to 4.3 +/- 0.4 mmHg but FENa did not significantly change (0.31 +/- 0.12 to 0.43 +/- 0.13%). In control SHRs (n = 7), at RPPs of 135 +/- 0.8 and 163 +/- 3.0 mmHg, RIHP was 4.4 +/- 0.4 and 5.0 +/- 0.6 mmHg (NS) and FENa was 0.41 +/- 0.10 and 0.82 +/- 0.17% (P less than 0.05). Renal decapsulation in the SHR did not affect the blunted relationships between RPP, RIHP, and FENa; at RPPs of 135 +/- 0.3 and 162 +/- 2.9 mmHg (n = 7), RIHP was 4.4 +/- 0.6 and 4.7 +/- 0.5 mmHg (NS) and FENa was 0.43 +/- 0.10 and 0.95 +/- 0.22% (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Direct measurement of renal medullary blood flow in the dog

1994 ◽  
Vol 267 (1) ◽  
pp. R253-R259 ◽  
Author(s):  
D. M. Strick ◽  
M. J. Fiksen-Olsen ◽  
J. C. Lockhart ◽  
R. J. Roman ◽  
J. C. Romero
Keyword(s):  
Blood Flow ◽  
Pressure Range ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Flow Probe ◽  
Renal Autoregulation ◽  
Renal Perfusion Pressure ◽  
Medullary Blood Flow ◽  
Renal Medullary Blood Flow ◽  
Doppler Flowmeter

We studied the responses of total renal blood flow (RBF) and renal medullary blood flow (RMBF) to changes in renal perfusion pressure (RPP) within and below the range of renal autoregulation in the anesthetized dog (n = 7). To measure RMBF, we developed a technique in which the medulla is exposed by excising a section of infarcted cortex and a multiple optical fiber flow probe, connected to a laser-Doppler flowmeter, is placed on the medulla. At the baseline RPP of 120 +/- 1 mmHg, RBF was 2.58 +/- 0.33 ml.min-1.g perfused kidney wt-1, and RMBF was 222 +/- 45 perfusion units. RPP was then decreased in consecutive 20-mmHg steps to 39 +/- 1 mmHg. At 80 +/- 1 mmHg, RBF remained at 89 +/- 4% of the baseline value; however, RMBF had decreased significantly (P < 0.05) to 73 +/- 4% of its baseline value. The efficiency of autoregulation of RBF and of RMBF within the RPP range of 120 to 80 mmHg was determined by calculating an autoregulatory index (AI) for each parameter using the formula AI = (%delta blood flow)/(%delta RPP). An AI of 0 indicates perfect autoregulation, and an index of 1 indicates a system with a fixed resistance. The AI for RBF averaged 0.33 +/- 0.12 over this pressure range and showed a significantly greater (P < 0.05) autoregulatory ability than did the RMBF (0.82 +/- 0.13). Decreasing perfusion pressure < 80 mmHg produced significant decreases in both RBF and RMBF.(ABSTRACT TRUNCATED AT 250 WORDS)

Mechanism of exaggerated diuresis in spontaneously hypertensive rats

1978 ◽  
Vol 235 (5) ◽  
pp. F409-F416 ◽  
Author(s):  
Gerald F. DiBona ◽  
Linda L. Rios
Keyword(s):  
Volume Expansion ◽  
Spontaneously Hypertensive Rats ◽  
Spontaneously Hypertensive Rat ◽  
Renal Perfusion ◽  
Sodium Reabsorption ◽  
Loop Of Henle ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Single Nephron ◽  
Wistar Kyoto

The mechanism of exaggerated diuresis and natriuresis was studied in spontaneously hypertensive rats (SHR) by renal clearance and micropuncture techniques. Control normotensive rats of the same age and sex [Wistar-Kyoto rats (WKY)] were also studied. During the hydropenic control and the volume-expansion experimental periods absolute and fractional water and sodium excretion were greater in SHR than in WKY. Although fractional and absolute water and sodium reabsorption were similar along the proximal convolution in SHR and WKY, fractional and absolute water reabsorption in Henle's loop was less in SHR than in WKY. Hydrostatic and colloid osmotic pressures in the cortical peritubular microvasculature were similar in WKY and SHR. Acute normalization of renal perfusion pressure by aortic constriction reversed the exaggerated diuresis and natriuresis in SHR by halving the filtered load of water and sodium; whole kidney and single nephron glomerular filtration rates and blood flows decreased by 50%. It is concluded that the exaggerated diuresis and natriuresis of the spontaneously hypertensive rat is caused by a decreased reabsorption in the loop of Henle. The mechanism of this decreased reabsorption in the loop of Henle cannot be explained by alterations in the measured physical forces in the renal cortical microvasculature. natriuresis; autoregulation; volume expansion Submitted on November 15, 1977 Accepted on June 7, 1978

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.

Short- and long-term enalapril affect renal medullary hemodynamics in the spontaneously hypertensive rat

1999 ◽  
Vol 276 (1) ◽  
pp. R10-R16 ◽  
Author(s):  
Stephen A. W. Dukacz ◽  
Michael A. Adams ◽  
Robert L. Kline
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Spontaneously Hypertensive Rat ◽  
Day Treatment ◽  
Ace Inhibition ◽  
Spontaneously Hypertensive ◽  
Short And Long Term ◽  
Pressure Natriuresis ◽  
The Relationship

Long-term angiotensin-converting enzyme (ACE) inhibition in the spontaneously hypertensive rat (SHR) resets pressure natriuresis and shifts the relationship between renal arterial pressure (RAP) and renal interstitial hydrostatic pressure (RIHP) to lower levels of arterial pressure. These effects persist after withdrawal of treatment. The purpose of this study was to determine the effect of short- and long-term ACE inhibition on medullary blood flow (MBF). Enalapril (25 mg ⋅ kg−1 ⋅ day−1in drinking water) was given to male SHR from 4 to 14 wk of age. Four weeks after stopping treatment, we measured MBF over a wide range of RAP using laser-Doppler flowmetry in anesthetized rats. Additional rats, either untreated or previously treated for 10 wk, received 3-day enalapril treatment just before the experiment. MAP (mmHg ± SE) was 178 ± 6 ( n = 8), 134 ± 6 ( n = 8), 138 ± 5 ( n = 9), and 111 ± 6 mmHg ( n = 9) for the untreated, 3 day, 10 wk, and 10 wk + 3 day groups, respectively. Total renal blood flow for the groups receiving 3-day treatment was significantly higher when compared with that in rats with an intact renin-angiotensin system. Three-day treatment had no effect on the relationship between RAP and RIHP, whereas that in rats receiving 10-wk treatment was shifted to lower levels of RAP by ∼30 mmHg. Both 10-wk and 3-day treatment independently increased the slope of the RAP versus MBF relationship at values of RAP > 100 mmHg. The slopes in perfusion units/mmHg were 0.12 ± 0.01 ( n = 8), 0.26 ± 0.01 ( n = 8), 0.27 ± 0.01 ( n = 9), and 0.30 ± 0.02 ( n = 9) for the untreated, 3 day, 10 wk, and 10 wk + 3 day groups, respectively. These results indicate that the effect of short-term and the persistent effect of long-term enalapril alter renal medullary hemodynamics in a way that may contribute to the resetting of the pressure-natriuresis relationship in treated rats.

Cerebral artery responses to pressure and flow in uremic hypertensive and spontaneously hypertensive rats

2003 ◽  
Vol 284 (4) ◽  
pp. H1212-H1216 ◽  
Author(s):  
D. I. New ◽  
A. M. S. Chesser ◽  
R. C. Thuraisingham ◽  
M. M. Yaqoob
Keyword(s):  
Blood Flow ◽  
Cerebral Artery ◽  
Spontaneously Hypertensive Rats ◽  
Perfusion Pressure ◽  
Hypertensive Rats ◽  
Independent Manner ◽  
Spontaneously Hypertensive ◽  
Cerebral Blood Flow Autoregulation ◽  
Wistar Kyoto ◽  
Normotensive Control

Impaired cerebral blood flow autoregulation is seen in uremic hypertension, whereas in nonuremic hypertension autoregulation is shifted toward higher perfusion pressure. The cerebral artery constricts in response to a rise in either lumen pressure or flow; we examined these responses in isolated middle cerebral artery segments from uremic Wistar-Kyoto rats (WKYU), normotensive control rats (WKYC), and spontaneously hypertensive rats (SHR). Pressure-induced (myogenic) constriction developed at 100 mmHg; lumen flow was then increased in steps from 0 to 98 μl/min. Some vessels were studied after endothelium ablation. Myogenic constriction was significantly lower in WKYU (28 ± 2.9%) compared with both WKYC (39 ± 2.5%, P = 0.035) and SHR (40 ± 3.1%, P = 0.018). Flow caused constriction of arteries from all groups in an endothelium-independent manner. The response to flow was similar in WKYU and WKYC, whereas SHR displayed increased constriction compared with WKYU ( P < 0.001) and WKYC ( P < 0.001). We conclude that cerebral myogenic constriction is decreased in WKYU, whereas flow-induced constriction is enhanced in SHR.

scholarly journals Altered renal hemodynamics and impaired myogenic responses in the fawn-hooded rat

1999 ◽  
Vol 276 (3) ◽  
pp. R855-R863 ◽  
Author(s):  
Richard P. E. van Dokkum ◽  
Cheng-Wen Sun ◽  
Abraham P. Provoost ◽  
Howard J. Jacob ◽  
Richard J. Roman
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Renal Damage ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Myogenic Response ◽  
Renal Perfusion Pressure ◽  
Medullary Blood Flow ◽  
Low Blood Pressure

The present study examined whether an abnormality in the myogenic response of renal arterioles that impairs autoregulation of renal blood flow (RBF) and glomerular capillary pressure (PGC) contributes to the development of renal damage in fawn-hooded hypertensive (FHH) rats. Autoregulation of whole kidney, cortical, and medullary blood flow and PGC were compared in young (12 wk old) FHH and fawn-hooded low blood pressure (FHL) rats in volume-replete and volume-expanded conditions. Baseline RBF, cortical and medullary blood flow, and PGCwere significantly greater in FHH than in FHL rats. Autoregulation of renal and cortical blood flow was significantly impaired in FHH rats compared with results obtained in FHL rats. Myogenically mediated autoregulation of PGC was significantly greater in FHL than in FHH rats. PGC rose from 46 ± 1 to 71 ± 2 mmHg in response to an increase in renal perfusion pressure from 100 to 150 mmHg in FHH rats, whereas it only increased from 39 ± 2 to 53 ± 1 mmHg in FHL rats. Isolated perfused renal interlobular arteries from FHL rats constricted by 10% in response to elevations in transmural pressure from 70 to 120 mmHg. In contrast, the diameter of vessels from FHH rats increased by 15%. These results indicate that the myogenic response of small renal arteries is altered in FHH rats, and this contributes to an impaired autoregulation of renal blood flow and elevations in PGC in this strain.

scholarly journals Cortical and medullary hemodynamics in deoxycorticosterone acetate-salt hypertensive mice.

1998 ◽  
Vol 9 (3) ◽  
pp. 346-354 ◽  
Author(s):  
V Gross ◽  
A Lippoldt ◽  
J Bohlender ◽  
M Bader ◽  
A Hansson ◽  
...  
Keyword(s):  
Blood Flow ◽  
Volume Expansion ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Kidney Weight ◽  
Cortical Blood Flow ◽  
Renal Perfusion Pressure ◽  
Medullary Blood Flow ◽  
Saline Loading ◽  
Baseline Values

The effect of acutely increasing renal perfusion pressure or extracellular fluid volume on renal medullary and cortical blood flow was examined in the low-renin deoxycorticosterone acetate (DOCA)-salt hypertension model in mice. A 50-mg DOCA tablet was implanted, and 1% saline was given as drinking water for 3 wk. Medullary and cortical blood flow were determined with laser-Doppler flowmetry, and whole-kidney blood flow was measured with a transit-time ultrasound flowprobe around the renal artery. In control mice, total renal blood flow ranged from 6.3 and 7.6 ml/min per g kidney weight and in DOCA-salt mice from 4.3 and 4.7 ml/min per g kidney weight, respectively, and was minimally affected as renal perfusion pressure was increased. Renal vascular resistance increased correspondingly. During stepwise increases in renal artery pressure from 90 to 140 mmHg, medullary blood flow progressively increased in control mice to 125% of baseline values, whereas cortical blood flow did not change. In DOCA-salt mice, increasing BP from 100 to 154 mmHg had no effect on either cortical or medullary blood flow. Urine flow and sodium excretion were lower in DOCA-salt mice than in controls and increased nearly to the same extent in both groups after volume expansion with isotonic saline. Total renal blood flow increased after saline loading, more in controls than in DOCA-salt mice. Increases in medullary blood flow after saline loading were up to 122% of baseline values in controls and demonstrated a significantly steeper slope than the 110% of baseline increases in DOCA-salt mice. Cortical blood flow, however, was not different between the groups. Thus, medullary blood flow is not as tightly autoregulated as cortical blood flow in normal mice. Natriuresis with acute volume loading is facilitated by increased medullary blood flow. In DOCA-salt mice, the medullary blood flow reaction to renal perfusion pressure increases is abolished, whereas flow increases with extracellular volume expansion are diminished. These results suggest that diminished pressure-natriuresis responses in DOCA-salt mice are related to perturbed medullary blood flow.

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.

Effects of renal artery pressure on interstitial pressure and Na excretion during renal vasodilation

1988 ◽  
Vol 255 (5) ◽  
pp. F828-F833 ◽  
Author(s):  
J. P. Granger ◽  
J. W. Scott
Keyword(s):  
Perfusion Pressure ◽  
Marked Effect ◽  
Excretion Rate ◽  
Fractional Excretion ◽  
Urinary Sodium Excretion ◽  
Renal Perfusion ◽  
Interstitial Pressure ◽  
Pressure Natriuresis ◽  
The Relationship

Renal vasodilation has a marked effect on the pressure-natriuresis relationship. The purpose of this study was to determine the role of renal interstitial hydrostatic pressure (RIHP) in mediating the effect of renal perfusion pressure (RPP) on urinary sodium excretion rate (UNaV) in control and vasodilated kidneys. The effects of RPP on UNaV and RIHP were determined in dogs under control conditions and during renal vasodilation with acetylcholine (Ach, 2.0 micrograms.kg-1.min-1) or secretin (SEC, 0.025 micrograms.kg-1.min-1). Decreases in RPP in control kidneys from 130 to 60 mmHg decreased UNaV from 2.9 +/- 0.1 to 0.6 +/- 0.3 microeq/min and fractional excretion of Na (FENa) from 0.15 +/- 0.08 to 0.06 +/- 0.04%. These changes were associated with significant reductions in RIHP (8.9 +/- 0.6 to 5.6 +/- 1.2 mmHg). In Ach-vasodilated kidneys, reductions in RPP from 130 to 60 mmHg decreased UNaV from 149.8 +/- 52.4 to 0.2 +/- 0.1 microeq/min and FENa from 3.42 +/- 1.18 to 0.012 +/- 0.01%. RIHP decreased from 17.8 +/- 3.4 to 8.4 +/- 1.3 mmHg, despite autoregulation of RBF. Renal vasodilation with SEC, which did not affect RIHP, had only a small effect on the relationship between RPP and UNaV. These data suggest that RIHP may be playing an important role in mediating the effect of RPP on UNaV.

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