Abstract
Phospholipase C (PLC) activation in neonatal rat ventricular cardiomyocytes (NRVM) generates inositol(1,4,5)trisphosphate (Ins(1,4,5)P 3) in response to elevations in Ca 2+ or inositol(1,4)bisphosphate in response to G protein stimulation. Overexpression of PLCδ 1 increased total [ 3H]inositol phosphate (InsP) content and elevated [ 3H]Ins(1,4,5)P 3, but failed to increase [ 3H]InsP responses to the Ca 2+ ionophore A23187. Antisense PLCδ 1 expression reduced endogenous PLCδ 1 content but did not decrease the A23187 response. In permeabilized NRVM, [ 3H]InsP responses to elevated Ca 2+ were not inhibited by Ins(1,4,5)P 3, even at concentrations 1000-fold greater than required for selective inhibition of PLCδ 1. Taken together these data provide evidence that PLCδ 1 does not mediate the InsP response to elevated Ca 2+ in NRVM.
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