Relationship between renin and intrarenal hemodynamics in hemorrhagic hypotension

A. Grandchamp; R. Veyrat; E. Rosset; J. R. Scherrer; B. Truniger

doi:10.1172/JCI106590

Relationship between renin and intrarenal hemodynamics in hemorrhagic hypotension

A. Grandchamp, R. Veyrat, E. Rosset, J. R. Scherrer, and B. Truniger

Published May 1, 1971 - More info

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Abstract

In order to investigate the possible role of the renin-angiotensin system in the regulation of intrarenal hemodynamics in hemorrhagic hypotension (HH), seven mongrel dogs have been studied under the following conditions: (a) Control, (b) HH (mean arterial pressure 70 mm Hg), and (c) HH + alpha adrenergic blockade by phenoxybenzamine (HH + POB). The following parameters were obtained for the right kidney: Intrarenal distribution of blood flow and local blood flow rates (¹³³Xe washout technique); total renal blood flow (RBF) on the basis of the clearance and extraction ratio of PAH and the arterial hematocrit; plasma renin concentrations in the renal artery and vein by the method of Boucher and his associates; and renin release into the renal circulation.

Alpha adrenergic blockade reverted the typical redistribution of intrarenal blood flow observed under HH. In hemorrhage, arterial and venous renin concentrations increased by a factor of 3.4 and 4.8 respectively. A further small increase was observed during HH + POB with the respective factors increasing to 4.8 and 5.3, as compared with control values. The renin release into the circulation increased by a factor of 1.2 in HH and 4.0 in HH + POB. Whereas in HH there seemed to be a relationship between increased renin concentrations or renin release, and the redistribution of blood flow, no such correlation was found during α-adrenergic blockade. From these observations it is concluded that renin alone is unable to maintain the typical redistribution of RBF seen during hemorrhage. Circumstantial evidence points to a permissive role of the renin-angiotensin system in the pathogenesis of the patchy cortical hypoperfusion caused by sympathoadrenergic mechanisms during hemorrhagic hypotension.

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