Stimulation of G‐protein coupled receptors in vascular smooth muscle cells induces tyrosine kinase dependent increases in calcium without tyrosine phosphorylation of phospholipase C γ‐1

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Abstract
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 β1 isoform of phospholipase C (PLC). However, recent studies showed that rat aortic VSMC do not express PLC β‐1 and that stimulation with angiotensin‐II induces tyrosine kinase dependent increases in [Ca2+]i and tyrosine phosphorylation of PLC γ‐1. Whether this pathway is activated by other vasoactive agents that stimulate G‐protein coupled receptors is unknown. Here, we show that A10 VSMC express PLC β‐2, PLC β‐3, PLC δ‐1, and PLC γ‐1. The cells also expressed Gαq/11. However, neither PLC β‐1 nor PLC β‐4 was detected. Stimulation with angiotensin‐II, vasopressin, serotonin, or endothelin induced tyrosine kinase dependent increases in [Ca2+]i. However, tyrosine phosphorylation of PLC γ‐1 did not occur. In contrast, stimulation with platelet derived growth factor increased [Ca2+]i and tyrosine phosphorylation of PLC γ‐1. The results show that tyrosine phosphorylation of PLC γ‐1 is not required for tyrosine kinase dependent increases in [Ca2+]i resulting from stimulation of diverse G‐protein coupled receptors in VSMC.