Search

Phospholipase C (PLC) activation in neonatal rat ventricular cardiomyocytes (NRVM) generates inositol(1,4,5)trisphosphate (Ins(1,4,5)P3) in response to elevations in Ca2+ or inositol(1,4)bisphosphate in response to G protein stimulation. Overexpression of PLCδ1 increased total [3H]inositol phosphate (InsP) content and elevated [3H]Ins(1,4,5)P3, but failed to increase [3H]InsP responses to the Ca2+ ionophore A23187. Antisense PLCδ1 expression reduced endogenous PLCδ1 content but did not decrease the A23187 response. In permeabilized NRVM, [3H]InsP responses to elevated Ca2+ were not inhibited by Ins(1,4,5)P3, even at concentrations 1000-fold greater than required for selective inhibition of PLCδ1. Taken together these data provide evidence that PLCδ1 does not mediate the InsP response to elevated Ca2+ in NRVM. [Copyright &y& Elsevier]