AJP - Renal Physiology, Vol 260, Issue 5 670-F679, Copyright © 1991 by American Physiological Society
Role of kinins and angiotensin II in the renal hemodynamic response to captopril
D. L. Mattson and R. J. Roman
Department of Physiology, Medical College of Wisconsin, Milwaukee 53226.
This study examined the role of angiotensin II (ANG II), kinins, and
prostaglandins in the renal hemodynamic response to captopril in
Munich-Wistar rats in which plasma renin activity was elevated [18.8 +/-
3.3 ng angiotensin I (ANG I).ml-1.h-1]. Neural influences on the kidney
were eliminated by renal denervation, and renal perfusion pressure (RPP)
was controlled using a clamp on the aorta. Urine flow, sodium excretion,
renal blood flow (RBF), glomerular filtration rate (GFR), and cortical and
papillary red blood cell (RBC) flow increased significantly after captopril
(2 mg/kg iv). Glomerular and peritubular capillary pressures rose by 20%,
and vasa recta capillary pressure fell by 3-4 mmHg due to significant
reductions in estimated preglomerular, efferent arteriolar and renal
capillary-venous vascular resistances. Infusion of ANG II (20 ng.kg-1.min-1
iv) returned RBF, GFR, and glomerular and peritubular capillary pressures
to control; however, ANG II did not lower papillary RBC flow before
inhibition of prostaglandin synthesis. Saralasin had no effect on papillary
RBC flow or the response to captopril. The changes in vasa recta
hemodynamics produced by captopril were blocked by a kinin antagonist.
These findings indicate that ANG II exerts a vasoconstrictor influence on
the renal cortical vasculature of Munich-Wistar rats; however, its effects
on the medullary circulation are opposed by vasodilatory eicosanoids. They
also suggest that kinins participate in the papillary RBC flow response to
captopril, perhaps by reducing the outflow resistance from the vasa recta
circulation.
