Control of rat renal vascular resistance during alterations in sodium balance.

Renal perfusion pressure (RPP), total renal blood flow (RBF), and renal vascular resistance (RVR) were comparable in groups of rats placed on high (HS) or low sodium (LS) diets for several weeks (HS, RVR = 16.4 ± 0.6; LS, RVR = 17.4 ± 0.6 mm Hg/ml per min). However, urinary kallikrein excretion was significantly lower in HS (0.31 ± 0.05U/min) than LS rats (0.98 ± 0.09U/min; P< 0.001). Studies reported here were performed to test the hypothesis that parallel changes in the kallikreinkinin system act to modify the vasoconstrictor effect of changes in the renin-angiotensin system in rats on varying sodium diets. In LS rats, saralasin, a competitive antagonist of angiotensin II (All) reduced RVR from 17.4 ± 1.1 to 12.7 ± 1.1 mm Hg /ml per min (P < 0.005), and captopril, a converting enzyme (kininase II) inhibitor, reduced RVR from 17.1 ± 1.0 to 10.8 ± 0.7 mm Hg/ml per min (P < 0.005). Captopril failed to reduce RVR when given to LS rats pretreated with saralasin, indicating that All inhibition probably is the mechanism of action of captopril in LS rats. Aprotinin, a kallikrein inhibitor, increased RVR from 17.5 ± 0.5 to 20.8 ± 0.9 mm Hg/ml per min in LS rats. Kinin infusion failed to reduce RVR in LS rats, but decreased RVR from 21.2 ± 1.7 to 17.6 ± 1.0 mm Hg/ml per min in aprotinintreated LS rats. Therefore, resistance to the vasodilator effect of kinins in LS rats probably is due to functionally maximal endogenous kinin levels. In HS rats, saralasin failed to reduce RVR, but captopril reduced RVR from 15.6 ± 0.9 to 12.3 ± 1.0 mm Hg/ml per min (P < 0.025). Since aprotinin blocked this effect of captopril, it was probably due to potentiation of kinins by inhibition of kininase II. In HS rats, aprotinin alone had no effect on RVR, whereas kinin infusion reduced resistance from 17.8 ± 1.6 to 13.5 ± 1.6 mm Hg/ml per min (P < 0.005). From these data we concluded that kinins and AH both exert significant control over RVR in LS, but not HS rats. The balance between these hormones may act to stabilize RVR during wide variations in sodium intake. Circ Res 48: 728-733, 1981