Effect of angiotensin II infusion in rats on Na,K-ATPase activity in renal cortical microsomal preparations

Direct dose-dependent effects of angiotensin II on renal tubular sodium reabsorption have been demonstrated. Alterations in tubular sodium reabsorption may occur via modulation of renal Na,K-ATPase activity. Thus, these experiments were undertaken to ascertain whether angiotensin II could influence renal cortical Na,K-ATPase activity. Angiotensin II, 495 ng/μl/h, or vehicle (controls) was infused for 24 h via miniosmotic pumps 48 h after rats were adrenalectomized and implanted with osmotic pumps containing 12.5 μg/μl corticosterone (Treatment I) or both corticosterone and 0.2 μg/μl aldosterone (Treatment II), and in rats receiving 3% NaCl in their food (sodium loaded, Treatment III). Rats receiving Treatments I and III received saline to drink. Renal cortical microsomal membranes were prepared, and the effects of angiotensin II infusion on the K _{1 2} and V_max for Na, K, and ATP determined. Angiotensin II infusions were associated with (i) a decrease (P < 0.001) in the K _{1 2} for Na activation of Na,K-ATPase from 14 ± 3 to 6 ± 1 (n = 4 experiments), 16 ± 1 to 12 ± 1 (n = 5), and 12 ± 3 to 7 ± 1 (n = 5) mm (means ± SE) for treatments I, II, and III, respectively; (ii) no changes in the K _{1 2} for K activation or the K_m for ATP; (iii) no changes in the V_max for Na, K, or ATP; and (iv) no change in Mg-ATPase activity. We conclude that angiotensin II infusion is associated with a decrease in the K _{1 2} of renal cortical Na,K-ATPase activity for sodium. This action of angiotensin II on the enzyme activity may contribute to the regulation of tubular sodium transport.