scholarly journals Pressure Natriuresis and Autoregulation of Inner Medullary Blood Flow in Canine Kidney

Hypertension ◽  
1997 ◽  
Vol 29 (1) ◽  
pp. 210-215 ◽  
Author(s):  
Dewan S.A. Majid ◽  
Murrell Godfrey ◽  
Sophia A. Omoro
Keyword(s):  
Blood Flow ◽  
Medullary Blood Flow ◽  
Pressure Natriuresis ◽  
Canine Kidney

Pressure Natriuresis and Renal Medullary Blood Flow in Dogs

Hypertension ◽  
1997 ◽  
Vol 29 (4) ◽  
pp. 1051-1057 ◽  
Author(s):  
Dewan S. A. Majid ◽  
Murrell Godfrey ◽  
L. Gabriel Navar
Keyword(s):  
Blood Flow ◽  
Medullary Blood Flow ◽  
Renal Medullary Blood Flow ◽  
Pressure Natriuresis

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.

scholarly journals Recovery from renal ischemia-reperfusion injury is associated with altered renal hemodynamics, blunted pressure natriuresis, and sodium-sensitive hypertension

2009 ◽  
Vol 297 (5) ◽  
pp. R1358-R1363 ◽  
Author(s):  
Kimberly R. Pechman ◽  
Carmen De Miguel ◽  
Hayley Lund ◽  
Ellen C. Leonard ◽  
David P. Basile ◽  
...  
Keyword(s):  
Blood Flow ◽  
Ischemia Reperfusion ◽  
Arterial Occlusion ◽  
Renal Ischemia ◽  
Interstitial Pressure ◽  
Kidney Weight ◽  
Doppler Flowmetry ◽  
Medullary Blood Flow ◽  
Arterial Blood ◽  
Pressure Natriuresis

The present studies evaluated intrarenal hemodynamics, pressure natriuresis, and arterial blood pressure in rats following recovery from renal ischemia-reperfusion (I/R) injury. Acute I/R injury, induced by 40 min of bilateral renal arterial occlusion, resulted in an increase in plasma creatinine that resolved within a week. Following 5 wk of recovery on a 0.4% NaCl diet, the pressure-natriuresis response was assessed in anesthetized rats in which the kidney was denervated and extrarenal hormones were administered intravenously. Increasing renal perfusion pressure (RPP) from 107 to 141 mmHg resulted in a fourfold increase in urine flow and sodium excretion in sham control rats. In comparison, pressure diuresis and natriuresis were significantly attenuated in post-I/R rats. In sham rats, glomerular filtration rate (GFR) averaged 1.6 ± 0.2 ml·min−1·g kidney weight−1 and renal blood flow (RBF) averaged 7.8 ± 0.7 ml·min−1·g kidney weight−1 at RPP of 129 mmHg. Renal cortical blood flow, measured by laser-Doppler flowmetry, was well autoregulated whereas medullary blood flow and renal interstitial hydrostatic pressure increased directly with elevated RPP in sham rats. In contrast, GFR and RBF were significantly reduced whereas medullary perfusion and interstitial pressure demonstrated an attenuated response to RPP in post-I/R rats. Further experiments demonstrated that conscious I/R rats develop hypertension when sodium intake is increased. The present data indicate that the pressure-natriuretic-diuretic response in I/R rats is blunted because of a decrease in GFR and RBF and the depressed pressure-dependent increase in medullary blood flow and interstitial pressure.

scholarly journals Impairment of pressure-natriuresis and renal autoregulation in ANG II-infused hypertensive rats

2000 ◽  
Vol 279 (2) ◽  
pp. F319-F325 ◽  
Author(s):  
Chi-Tarng Wang ◽  
So Yeon Chin ◽  
L. Gabriel Navar
Keyword(s):  
Blood Flow ◽  
Renal Plasma Flow ◽  
Left Renal Artery ◽  
Concomitant Treatment ◽  
Ang Ii ◽  
Hypertensive Rats ◽  
Simultaneous Treatment ◽  
Renal Autoregulation ◽  
Medullary Blood Flow ◽  
Pressure Natriuresis

Chronic infusions of initially subpressor doses of angiotensin II (ANG II) lead to progressive hypertension over a 2-wk period and to augmented intrarenal ANG II levels. The present study was performed to investigate total renal blood flow (RBF) and medullary blood flow (MBF) autoregulatory behavior and pressure-natriuresis in ANG II-infused hypertensive rats and how these are modified by concomitant treatment with an ANG II AT1 receptor antagonist. ANG II-infused rats ( n = 27) were prepared by administration of ANG II at 60 ng/min via osmotic minipump for 13 days. Twelve of the ANG II-infused hypertensive rats were treated with losartan in the drinking water (30 mg · kg ·−1 day−1). Rats were anesthetized with pentobarbital sodium (50 mg/kg, ip) and prepared for renal function measurements. An aortic clamp was placed above the junction of the left renal artery to reduce renal arterial pressure. Autoregulatory responses for renal plasma flow, overall RBF, and glomerular filtration rate were impaired in ANG II-infused hypertensive rats; however, MBF autoregulation was not disrupted. Most strikingly, pressure-natriuresis was markedly suppressed in ANG II-infused hypertensive rats. Chronic treatment with losartan prevented the impairment of the pressure-natriuresis relationship caused by chronic ANG II infusion. These findings demonstrate that chronic ANG II infusion leads to marked impairment of sodium excretion and suppression of the pressure-natriuresis relationship, which may contribute to the progressive hypertension that occurs in this model. These renal effects are prevented by simultaneous treatment with an AT1receptor blocker.

scholarly journals Dominant factors that govern pressure natriuresis in diuresis and antidiuresis: a mathematical model

2014 ◽  
Vol 306 (9) ◽  
pp. F952-F969 ◽  
Author(s):  
Robert Moss ◽  
Anita T. Layton
Keyword(s):  
Blood Flow ◽  
Collecting Duct ◽  
Proximal Convoluted Tubule ◽  
Tubuloglomerular Feedback ◽  
Hydration Status ◽  
Renal Autoregulation ◽  
Medullary Blood Flow ◽  
Collecting Duct Epithelium ◽  
Pressure Natriuresis ◽  
Solute Composition

We have developed a whole kidney model of the urine concentrating mechanism and renal autoregulation. The model represents the tubuloglomerular feedback (TGF) and myogenic mechanisms, which together affect the resistance of the afferent arteriole and thus glomerular filtration rate. TGF is activated by fluctuations in macula densa [Cl−] and the myogefnic mechanism by changes in hydrostatic pressure. The model was used to investigate the relative contributions of medullary blood flow autoregulation and inhibition of transport in the proximal convoluted tubule to pressure natriuresis in both diuresis and antidiuresis. The model predicts that medullary blood flow autoregulation, which only affects the interstitial solute composition in the model, has negligible influence on the rate of NaCl excretion. However, it exerts a significant effect on urine flow, particularly in the antidiuretic kidney. This suggests that interstitial washout has significant implications for the maintenance of hydration status but little direct bearing on salt excretion, and that medullary blood flow may only play a signaling role for stimulating a pressure-natriuresis response. Inhibited reabsorption in the model proximal convoluted tubule is capable of driving pressure natriuresis when the known actions of vasopressin on the collecting duct epithelium are taken into account.

Role of Nitric Oxide on Papillary Blood Flow and Pressure Natriuresis

Hypertension ◽  
1995 ◽  
Vol 25 (3) ◽  
pp. 408-414 ◽  
Author(s):  
Francisco J. Fenoy ◽  
Paloma Ferrer ◽  
Luis Carbonell ◽  
Miguel García-Salom
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Pressure Natriuresis

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.

The local xenon washout method applied to the study of blood flow in subcapsular cortex of the canine kidney

1983 ◽  
Vol 396 (2) ◽  
pp. 182-183 ◽  
Author(s):  
Ulrik Abildgaard ◽  
O. Amtorp ◽  
S. Hans� ◽  
P. Rosenkilde ◽  
P. Sejrsen
Keyword(s):  
Blood Flow ◽  
Xenon Washout ◽  
Canine Kidney
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