MERCURY-CHLORIDE AS A POSSIBLE PHOSPHOLIPASE-C ACTIVATOR - EFFECT ON ANGIOTENSIN-II-INDUCED [CA++]I TRANSIENT IN THE RAT EARLY PROXIMAL TUBULE

In our previous report (Biochem. Biophys. Res. Commun. 165(3), 1221-1228, 1989), we have demonstrated the biphasic increase of intracellular free calcium concentration ([Ca++]i) induced by angiotensin II (ANG II) in isolated rat early proximal tubule (S1). The present study was undertaken to determine the effect of HgCl2 on ANG II-induced [Ca++]i increase using Fura-2. HgCl2 (10-10M2 - 10-8M) potentiated the [Ca++]i increase induced by ANG II (10-11M) in a dose-dependent manner. To determine the mechanism of stimulatory effect by HgCl2 on ANG II-induced [Ca++]i increase, nephron segments were pretreated with 10-4M propranolol, a phospholipase C inhibitor. The stimulatory effect by 10-9M HgCl2 in 10-11M ANG II-induced [Ca++]i increase was completely inhibited by propranolol. Moreover, 10-4M propranolol completely blocked the stimulatory effect of HgCl2 on ANG II-mediated IP3 production. This study suggests for the first time that HgCl2 stimulates the [Ca++]i increment induced by ANG II, possibly through an activation of phospholipase C. © 1990 Academic Press, Inc.