POTENTIATION BY ALDOSTERONE OF VASOPRESSIN-INDUCED CALCIUM KINETICS IN VASCULAR SMOOTH MUSCLE CELLS

Abstract

1. The present study was undertaken to examine the effect of aldosterone on arginine vasopressin (AVP)-induced Ca2+ kinetics in cultured rat vascular smooth muscle cells (VSMC). The pre-incubation of cells with 1 x 10(-6) mol/L aldosterone for 24 h did not affect the basal cytosolic free Ca2+ [( Ca2+]i) but enhanced the AVP-induced mobilization of [Ca2+]i (1 x 10(-8) mol/L AVP; 287 vs 401, 1 x 10(-6) mol/L AVP; 430 vs 714 nmol/L). 2. The pre-incubation of cells with 1 x 10(-7) mol/L aldosterone for 24 h did not show this enhancing effect on the AVP-induced mobilization of [Ca2+]i. Without the preincubation, aldosterone did not change the basal [Ca2+]i or the AVP-induced mobilization of [Ca2+]i. This enhancement was still observed in the Ca2+-free solution containing 0.1 mmol/L EGTA (1 x 10(-8) mol/L AVP; 169 vs 341 nmol/L). 3. The enhancement by aldosterone of the AVP-mobilized [Ca2+]i was completely blocked by the simultaneous administration of 1 x 10(-4) mol/L spironolactone (1 x 10(-8) mol/L AVP; 258 vs 265 nmol/L). The treatment with aldosterone also stimulated the AVP-produced [45Ca2+] efflux during a 3 min period (1 x 10(-8) mol/L AVP; 32 vs 49, 1 x 10(-6) mol/L AVP; 50 vs 58% released from the resting intracellular [45Ca2+]-contents). 4. The present results indicate that aldosterone enhances the vascular action of AVP mediated through the stimulation of Ca2+ kinetics which may be dependent on the changes in the cellular signal transduction systems.