Abstract

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.

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