Control of rat renal vascular resistance at reduced perfusion pressure.

Determination of the factors influencing renal vascular resistance (RVR) at very low perfusion pressures (RPP) is of interest, since prolonged periods of reduced perfusion can lead to acute renal failure. We have studied the effects of inhibition of the renin-angiotensin system on renal blood flow (RBF), measured by electromagnetic flow probe, over a subautoregulatory pressure range of BOSS mm Hg. These studies were carried out in rats on low sodium diets (LS), in which angiotensin II (All) is increased, and high sodium diets (HS), in which All is suppressed. We have also studied the effect of altering the kallikrein-kinin system, since our previous studies have indicated an interaction between this system and All in control of RVR at normal RPP. Variations in sodium intake did not alter the regression of RBF on RPP over the entire low pressure range.. RVR in LS rats increased from 15.8 ± 0.4 between 65 and 90 mm Hg to 21.2 ± 1.2 mm Hg/ml per min at pressures <45 mm Hg (P < 0.05). In HS rats, RVR rose from 13.8 ± 0.5 at RPP between 65 and 90 mm Hg to 18.6 ± 0.9 mm Hg/ml per min at RPP < 45 mm Hg (P < 0.001). Saralasin, an All antagonist, increased RBF, and thus reduced RVR, over the entire low pressure range in LS rats, but had no effect on RVR in HS rats. Captopril, which inhibits the formation of All as well as the degradation kinins, increases RBF in both LS and HS rats. Aprotinin, an inhibitor of kallikrein, reduced RBF, and thus increased RVR over the entire low pressure range in LS rats. Aprotinin had no effect on RVR in HS rats, but pretreatment with this agent blocked the vasodilatory effect of captopril. Infusion of kinins raised RBF in HS rats but had no effect on RBF of LS rats. We conclude that RVR is not fixed or minimal in the subautoregulatory pressure range. AH acts as a vasoconstrictor throughout this low pressure range in LS rats, but its effect is countered by the vasodilator influence of kinins. Neither hormone substantially influenced RVR in HS rats. Parallel changes in the activity of these two hormones maintains a relatively constant RVR despite changes in dietary sodium intake. CircRes 48: 734-739, 1981