STIMULATION OF G-PROTEIN COUPLED RECEPTORS IN VASCULAR SMOOTH-MUSCLE CELLS INDUCES TYROSINE KINASE-DEPENDENT INCREASES IN CALCIUM WITHOUT TYROSINE PHOSPHORYLATION OF PHOSPHOLIPASE-C GAMMA-1

It is often believed that increases in intracellular Ca2+ ([Ca2+](i)) resulting from stimulation of G-protein coupled receptors in vascular smooth muscle cells (VSMC) require activation of the beta 1 isoform of phospholipase C (PLC). However, recent studies showed that rat aortic VSMC do not express PLC beta 1 and that stimulation with angiotensin- II induces tyrosine kinase dependent increases in [Ca2+](i) and tyrosi ne phosphorylation of PLC gamma-1, Whether this pathway is activated b y other vasoactive agents that stimulate G-protein coupled receptors i s unknown. Here, we show that A10 VSMC express PLC beta-2, PLC beta-3, PLC delta-1, and PLC gamma-1, The cells also expressed G alpha(q)/11. However, neither PLC beta-1 nor PLC beta-4 was detected, Stimulation with angiotensin-II, vasopressin, serotonin, or endothelin induced tyr osine kinase dependent increases in [Ca2+](i). However, tyrosine phosp horylation of PLC gamma-1 did not occur, In contrast, stimulation with platelet derived growth factor increased [Ca2+](i) and tyrosine phosp horylation of PLC gamma-1, The results show that tyrosine phosphorylat ion of PLC gamma-1 is not required for tyrosine kinase dependent incre ases in [Ca2+](i) resulting from stimulation of diverse G-protein coup led receptors in VSMC. (C) 1998 Federation of European Biochemical Soc ieties.