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In 10 dogs in each of which one kidney was left intact, unilateral renal artery constriction (R.A.C.) resulted in an increase in aortic pressure (PA) for as long as 13 months. When PA had stabilized at 156 ± 14 mm Hg compared with a baseline of 128 ± 13 mm Hg (p < 0.001) urine flow rate (V), sodium excretion (UNaV), and chloride excretion (UClV) decreased in the constricted kidney (E), while creatinine clearance (CCr) and para-aminohippurate clearance (CPAH) did not change significantly. In the contralateral control kidney (C) V, UNaV, and UClV increased, in association with increases in CCr and CPAH, but without changes in filtration fraction or renal vascular resistance. Although E/C creatinine concentration (UCr) increased as E/C V fell, E/C urine sodium concentration remained unchanged. However, when differences in V, UNaV, UClV, CCr, CPAH, and UCr between C and E were enhanced in relation to a transient exaggerated increase in PA in the acute phase following R.A.C., E/C UNa appeared to decrease slightly. When collateral circulation which had developed to E was stripped, enhanced differences in separate renal function recurred in association with a further increase in PA. Thus, chronic R.A.C. leads to the development of collateral renal circulation which appears responsible for improvement in function in E, and decrease in PA. These effects are associated with decrease in function on the control side, thereby leading to a reduction in differences in function between the two sides.

During induced renal vasodilatation, angiotensin and norepinephrine result in an increased excretion of sodium (UNaV), which has been attributed to transmission of elevated aortic pressure (PA) to peritubular capillaries and not to direct effects of the drugs on sodium reabsorption. The importance of PA, intrarenal hemodynamics, and other possible effects of angiotensin and norepinephrine was examined in anesthetized dogs in which one kidney was vasodilated by denervation or acetylcholine, and the opposite kidney served as control. During elevation of aortic pressure, following bilateral carotid occlusion and vagotomy (B.C.O. and V), infusion of angiotensin and norepinephrine, increased UNaV occurred on only the vasodilated side. Changes in UNaV on both sides are related inversely to renal vascular resistance (R.V.R.) before elevation PA, but not to changes in R.V.R., glomerular filtration rate (G.F.R.), or filtration fraction following elevation of PA. When renal perfusion pressure was controlled during aortic constriction, persistent increases in UNaV and urine flow rate were abolished during infusion of norepinephrine and after B.C.O. and V, and markedly reduced during infusion of angiotensin. These effects could not be attributed to changes in intrarenal hemodynamics. Thus increased sodium and water excretion following infusion of norepinephrine and angiotensin, and B.C.O. and V, can be largely attributed to an interplay of increased renal perfusion pressure and reduced preset renal vascular resistance.

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