Autoregulation of renal blood flow, glomerular filtration rate and renin release in conscious dogs

1987 ◽  
Vol 410 (4-5) ◽  
pp. 441-449 ◽  
Author(s):  
H. R. Kirchheim ◽  
H. Ehmke ◽  
E. Hackenthal ◽  
W. Löwe ◽  
P. Persson
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Filtration Rate ◽  
Conscious Dogs ◽  
Renin Release

Adenosine-induced decrease in renin release: dissociation from hemodynamic effects

1984 ◽  
Vol 247 (3) ◽  
pp. F447-F452 ◽  
Author(s):  
L. J. Arend ◽  
A. Haramati ◽  
C. I. Thompson ◽  
W. S. Spielman
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Filtration Rate ◽  
Control Level ◽  
Hemodynamic Response ◽  
Renin Release ◽  
Adenosine Infusion ◽  
Hemodynamic Effects

Adenosine has been reported to produce a biphasic renal blood flow (RBF) response (vasoconstriction followed by a return of flow to control level) and a decrease in glomerular filtration rate (GFR) when infused into the kidney. Intrarenal adenosine infusion also leads to a decrease in renin release. By altering the hemodynamic response to adenosine, we sought to determine whether the decrease in renin release depends on vascular or filtration-induced events. In nine dogs with nonfiltering kidneys, adenosine infusion (3 X 10(-7) mol/min) resulted in a biphasic RBF response and an inhibition of renin release (309 +/- 53 vs. 71 +/- 26 ng ANG I/min). In 11 dogs treated with verapamil (10 micrograms X kg-1 X min-1) no vasoconstriction or decrease in GFR occurred; however, renin release was inhibited by adenosine (1,300 +/- 159 vs. 534 +/- 225 ng ANG I/min). In a third group of nine dogs whose ureteral pressure was raised to 80 cmH2O, adenosine infusion produced a sustained vasoconstriction and an inhibition of renin release (3,086 +/- 1,144 vs. 328 +/- 130 ng ANG I/min). These experiments, in which the renin release effects of adenosine are dissociated from the hemodynamic effects, lead us to conclude that the inhibition of renin release produced by adenosine does not depend either on the vascular or filtration-induced effects of adenosine.

A proposed role for adenosine in the regulation of renal hemodynamics and renin release

1982 ◽  
Vol 242 (5) ◽  
pp. F423-F435 ◽  
Author(s):  
W. S. Spielman ◽  
C. I. Thompson
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Filtration Rate ◽  
Renal Tissue ◽  
Renin Release ◽  
Organ Blood Flow ◽  
Arteriolar Resistance ◽  
Regional Renal Blood Flow

Adenosine is produced by renal tissue and has potent effects on renal blood flow and its distribution, glomerular filtration rate (GFR), and the secretion of renin. Intrarenal infusion of adenosine decreases GFR primarily by decreasing glomerular hydrostatic pressure through its effects in increasing afferent arteriolar resistance and possibly decreasing efferent arteriolar resistance. The fall in GFR due to adenosine is accompanied by little change or an increase in total organ blood flow. Regional renal blood flow during adenosine infusion is redistributed, with a greater percentage of total flow going to the juxtamedullary cortex. Intrarenal adenosine produces marked decreases in water and sodium excretion that are proportionally greater than its effect on GFR, suggesting a possible direct tubular action. Intrarenal adenosine also produces a rapid and pronounced inhibition of renin release that appears to be independent of its hemodynamic or tubular effects. A metabolic hypothesis for the control of glomerular filtration rate and renin release with adenosine acting as a mediator is considered, and criteria for establishing an intrarenal role for adenosine in the regulation of renal function are discussed.

Genetic co-segregation of renal haemodynamics and blood pressure in the spontaneously hypertensive rat

1988 ◽  
Vol 74 (1) ◽  
pp. 63-69 ◽  
Author(s):  
S. B. Harrap ◽  
A. E. Doyle
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Filtration Rate ◽  
Spontaneously Hypertensive Rat ◽  
Plasma Renin ◽  
Spontaneously Hypertensive

1. To determine the relevance of renal circulatory abnormalities found in the immature spontaneously hypertensive rat (SHR) to the genetic hypertensive process, glomerular filtration rate and renal blood flow were measured in conscious F2 rats, derived from crossbreeding SHR and normotensive Wistar–Kyoto rats (WKY), at 4, 11 and 16 weeks of age by determining the renal clearances of 51Cr-ethylenediaminetetra-acetate and 125I-hippuran respectively. Plasma renin activity was measured at 11 and 16 weeks of age. 2. Mean arterial pressure, glomerular filtration rate and renal blood flow increased between 4 and 11 weeks of age. Between 11 and 16 weeks the mean glomerular filtration rate and renal blood flow did not alter, although the mean arterial pressure rose significantly. At 11 weeks of age, during the developmental phase of hypertension, a significant negative correlation between mean arterial pressure and both glomerular filtration rate and renal blood flow was noted. However, by 16 weeks when the manifestations of genetic hypertension were more fully expressed, no correlation between mean arterial pressure and renal blood flow or glomerular filtration rate was observed. Plasma renin activity was negatively correlated with both glomerular filtration rate and renal blood flow, but the relationship was stronger at 11 than at 16 weeks of age. 3. These results suggest that the reduction in renal blood flow and glomerular filtration rate, found in immature SHR, is genetically linked to the hypertension and may be of primary pathogenetic importance. It is proposed that the increased renal vascular resistance in these young animals stimulates the rise of systemic arterial pressure which returns renal blood flow and glomerular filtration rate to normal.

Renal Blood Flow, Glomerular Filtration Rate, and Renal Oxygenation in Early Clinical Septic Shock*

2018 ◽  
Vol 46 (6) ◽  
pp. e560-e566 ◽  
Author(s):  
Jenny Skytte Larsson ◽  
Vitus Krumbholz ◽  
Anders Enskog ◽  
Gudrun Bragadottir ◽  
Bengt Redfors ◽  
...  
Keyword(s):  
Septic Shock ◽  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Filtration Rate

Use of a thermal pulse decay system to assess avian renal blood flow during reduced renal arterial perfusion pressure

1992 ◽  
Vol 262 (1) ◽  
pp. R90-R98 ◽  
Author(s):  
R. F. Wideman ◽  
R. P. Glahn ◽  
W. G. Bottje ◽  
K. R. Holmes
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Regional Differences ◽  
Filtration Rate ◽  
Perfusion Pressure ◽  
Portal Flow ◽  
Arterial Perfusion ◽  
Restricted Group

Using a simplified avian kidney model, renal arterial perfusion pressure (RAPP) was reduced from 120 (control) to 70 mmHg (near the glomerular filtration rate autoregulatory limit) and then to 46 mmHg (below the glomerular filtration rate autoregulatory range) in kidneys with ambient or partially restricted renal portal flow. Renal blood flow (RBF) was measured with a thermal pulse decay (TPD) system, using TPD thermistor probes inserted at three locations to evaluate regional differences in RBF. The clearance (CPAH) and extraction of p-aminohippuric acid were used to calculate renal plasma flow (RPF). CPAH, RPF, and RBF values were consistently lower for kidneys with restricted portal flow than for kidneys with ambient portal flow. Reducing RAPP to 46 mmHg did not significantly reduce CPAH, RPF, or RBF in the ambient group but did significantly reduce CPAH and RPF (regressed on RAPP) in the restricted group. RBF was not significantly affected when RAPP was reduced in the restricted group, although significant regional differences in blood flow were recorded. Renal vascular resistance decreased significantly as RAPP was reduced to 46 mmHg in the ambient group, confirming the renal autoregulatory response. In separate validation studies, significant reductions in RBF were detected by the TPD system during acute obstructions of portal and/or arterial flow. Overall, the results support previous evidence that avian RBF remains constant over a wide range of RAPPs. Observations of nonuniform intrarenal distributions of portal blood flow suggest that the portal system maintains the constancy of RBF in regions with proportionately high portal-to-arterial flow ratios.

Sign in / Sign up

Export Citation Format

Share Document