Effect of left atrial to left femoral artery bypass and renin-angiotensin system blockade on renal blood flow and function during and after thoracic aortic occlusion

1987 ◽  
Vol 5 (2) ◽  
pp. 329-335 ◽  
Author(s):  
Axel W. Joob ◽  
Cary Dunn ◽  
Ed Miller ◽  
Arthur Freedlender ◽  
Irving L. Kron
1975 ◽  
Vol 229 (4) ◽  
pp. 983-988 ◽  
Author(s):  
PA Jose ◽  
LM Slotkoff ◽  
S Montgomery ◽  
PL Calcagno ◽  
G Eisner

The ability of the immature kidney to autoregulate blood flow was investigated. Renal blood flow was measured by electromagnetic flowmeter. In six puppies, selective blockade of the intrarenal effects of angiotensin II (AII) by [1-sarcosine, 8-alanine]angiotensin II (anti-AII) administered into the renal artery did not change renal blood flow. During selective renal AII blockade, intravenous AII raised perfusion pressure from 76 +/- 2 to 100 +/- 6 mmHg. Renal blood flow increased from 1.59 +/- 0.29 to 1.98 +/- 0.59 ml/g kidney per min, but returned to control levels within 40 s in spite of persistent arterial pressure elevation. In another group of seven puppies, renal blood flow remained constant despite reduction of renal perfusion pressure by aortic constriction to 60 mmHg. In two of these seven puppies intrarenal anti-AII did not abolish autoregulation. Autoregulation of renal blood flow occurs in the puppy and is not influenced by inhibition of angiotensin. The renin-angiotensin system does not appear to be involved in the normal regulation of renal blood flow in the puppy.


1977 ◽  
Vol 9 (1) ◽  
pp. 48
Author(s):  
E. J. Zambraski ◽  
G. F. DIBona ◽  
C. M. Tipton ◽  
Edward J. Zambraski

1982 ◽  
Vol 62 (1) ◽  
pp. 35-41 ◽  
Author(s):  
E. Ståhl ◽  
B. E. Karlberg ◽  
L. Rammer

1. Intravascular coagulation in the kidneys of rats was induced by intravenous infusion of thrombin and by inhibition of fibrinolysis with tranexamic acid under α-chloralose anaesthesia. The amount of fibrin in the kidneys was measured with radioactively labelled fibrinogen. Chronic saline loading and inhibition of angiotensin II (ANG II) with saralasin reduced the fibrin deposition in the kidneys. Infusion of ANG II had the opposite effect. 2. Renal and aortic blood flows were measured by injection of radioactively labelled microspheres. After thrombin infusion the renal and aortic blood flows were reduced to about one-third of the pre-infusion values. Chronic saline loading diminished these changes, but saralasin had no effect. 3. Plasma renin activity (PRA), measured by radioimmunoassay, decreased by about 50% after thrombin infusion. 4. The reduction in PRA and the lack of effect of saralasin indicate that the renin—angiotensin system is not the mediator of the observed decrease in the renal blood flow. As saralasin reduced the amount of fibrin the mechanism regulating fibrin deposition appears to be independent of the mechanism that reduces the renal blood flow.


1976 ◽  
Vol 231 (4) ◽  
pp. 1267-1271 ◽  
Author(s):  
Y Abe ◽  
T Kishimoto ◽  
K Yamamoto

The role of the renin-angiotensin system in the autoregulation of renal blood flow was examined in the anesthetized dog. The angiotensin II antagonist, [1-sarcosine, 8-isoleucine]angiotensin II, was continuously infused into the renal artery at rates of 1 and 3 mug/min, and renin secretion rate and intrarenal distribution of blood flow as well as total renal blood flow were measured during acute reductions in renal perfusion pressure within and below the range of autoregulation. Renal autoregulation and redistribution of blood flow by pressure reduction were not disturbed by the angiotensin II antagonist. This result does not provide any evidence for a primary role of the renin-angiotensin system in renal autoregulation. Redistribution of blood flow by pressure reduction occurred independently of the renin-angiotensin system. It might depend on the differences in the resting tone among the zones.


1991 ◽  
Vol 261 (1) ◽  
pp. F51-F59 ◽  
Author(s):  
G. P. Brown ◽  
R. C. Venuto

Renal blood flow (RBF) was measured in conscious rabbits while nonpregnant and during pregnancy using chronically implanted ultrasonic transit-time flow probes. The effects of the cyclooxygenase inhibitor meclofenamate (5 mg/kg) and the angiotensin-converting-enzyme inhibitor captopril (5 mg/kg) on basal RBF and on RBF responses to systemic angiotensin II infusions (2.5-80 ng.kg-1.min-1) were determined. Basal RBF declined (P less than 0.001 to P less than 0.005) with meclofenamate by 9-16% in pregnant (n = 7) and by 10% in nonpregnant (n = 7) rabbits. Captopril increased (P less than 0.05 to P less than 0.01) RBF by 9-11% in pregnant (n = 5) and by 12% in nonpregnant (n = 5) rabbits. There was no effect of the vehicle (normal saline) on RBF. The reduction in RBF (% from baseline) in response to infused angiotensin II was attenuated in pregnant compared with nonpregnant rabbits. Pretreatment with meclofenamate enhanced the renal vasoconstrictor action of angiotensin II in a similar fashion in both pregnant and nonpregnant rabbits. Captopril or saline did not alter the RBF responses to angiotensin II infusions. Mean arterial pressure was lower in pregnant (78 +/- 3 mmHg, n = 7) vs. nonpregnant (88 +/- 5 mmHg, n = 10) rabbits, suggesting lower total peripheral resistance. The data indicate 1) chronically implanted ultrasonic flow probes can be an effective tool for monitoring RBF in conscious rabbits, 2) prostaglandins and the renin-angiotensin system influence basal RBF in conscious rabbits, and 3) the renal vasoconstrictor effect of angiotensin II is blunted in pregnant rabbits and this attenuated response appears to be independent of prostaglandins.


1977 ◽  
Vol 233 (4) ◽  
pp. F290-F297 ◽  
Author(s):  
W. J. Arendshorst ◽  
W. F. Finn

Renal blood flow (RBF) was measured with a noncannulating electromagnetic flow transducer in anesthetized rats which had been maintained for 3-5 wk on low, normal, or high salt plus deoxycorticosterone diets. After base-line observations, one of two dissimilar inhibitors of the renin-angiotensin system, angiotensin I converting enzyme inhibitor SQ 20881 or the structural analogue [Sar1,Ala8]angiotensin II was administered intravenously. The employed doses of SQ 20881 and [Sar1,Ala8]angiotensin II effectively inhibited the pressor and renal vasoconstrictor responses induced by exogenous angiotensin I and II, respectively, in each dietary group. Both inhibitors vasodilated kidneys in salt-restricted rats; however, neither affected base-line renal hemodynamics in salt-loaded rats. Pressure-flow relationships were evaluated by clamping the aorta to reduce renal perfusion pressure. Renal blood flow was autoregulated between 100 and 140 mmHg with the same efficiency before and during inhibition of angiotensin II in each dietary group. These data indicate that angiotensin II modifies base-line RBF and renal vascular resistance and are consistent with the view that the renin-angiotensin system is not an essential mechanism responsible for autoregulation of RBF in the rat.


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