Arginine vasopressin increases the rate of protein synthesis in isolated perfused adult rat heart via the V-1 receptor

Arginine vasopressin (AVP) is known to contribute significantly to the path ogenesis of congestive heart failure and hypertension. However, little is k nown about its effect on the myocardium. The present study was conducted to determine whether AVP directly increases the rate of protein synthesis in isolated, perfused rat heart, and, if so, the mechanism involved. Elevation of the aortic pressure from 60 to 120 mmHg in perfused rat heart accelerat ed the rate of protein synthesis which was associated with increases in cAM P levels and Ca2+ uptake. AVP (100 mu M) increased Ca2+ uptake and accelera ted the rate of protein synthesis without a change in cAMP concentration. T he latter events were inhibited by OPC-21268 (100 mu M), a selective V-1 re ceptor antagonist, or amiloride (100 mu M), an inhibitor of the Na+/H+ exch ange system. However, increases in cAMP concentrations, Ca2+ uptake, and ra tes of protein synthesis associated with the elevated aortic pressure were not inhibited by amiloride. Thus, AVP directly increased the rate of protei n synthesis via the V-1 receptor that is sensitive to amiloride, a mechanis m that differs from the cAMP-dependent mechanism that is responsible for th e cardiac hypertrophy induced by pressure overload.