PRESSOR RESPONSES FOLLOWING SHORT, COMPLETE RENAL ISCHEMIA: CHARACTERISTICS, MECHANISM, SPECIFICITY FOR KIDNEY

Abstract

Changes in blood pressure following restoration of renal circulation after periods (1/2-7 hrs.) of complete ischemia were studied in dogs anesthetized with chloralose. The circulation of both kidneys was interrupted by first destroying collateral circulation and then occluding the renal arteries and veins by clamps, which could be operated after closure of the abdomen. Prolonged pressor responses, persisting for the duration of these acute expts., uniformly resulted upon release of the clamps, even after intervals of ischemia as short as 1/2 hr. There was often a temporary rise and fall of blood pressure, preceding the sustained elevation. The possibility of nervous mechanisms was excluded by 4 groups of expts.: 1. manipulation of the clamps; 2. opening of the clamps with the renal vessels ligated and the accompanying nerve plexuses intact; 3. complete ischemia with the kidneys and their vessels denervated; 4 complete ischemia with the thoracolumbar cord destroyed and the vagi cut. The responses must, therefore, be due to pressor material from the ischemic kidney. This material does not exert its pressor action solely, if at all, through the C. N. S. Neither recent adrenalectomy nor splenectomy prevented the phenomenon. Unilateral, as well as bilateral, renal ischemia resulted in pressor responses. Complete ischemia of leg or liver was followed by either a fall or no change in blood pressure.