Inositol phospholipids localized to caveolae in rat heart are regulated by alpha1-adrenergic receptors and by ischemia-reperfusion.

Postischemic reperfusion of rat or mouse hearts causes generation of inositol (1,4,5)trisphosphate [Ins(1,4,5)P3] and the initiation of arrhythmias. In the current study we investigated the possibility that the enhanced Ins(1,4,5)P3 generation in postischemic reperfusion was associated with an increased availability of the precursor lipid phosphatidylinositol(4,5)bisphosphate (PIP2) for alpha1-adrenergic receptor-activated phospholipase C (PLC). Isolated-perfused rat hearts were labeled with [3H]inositol and subjected to ischemia-reperfusion or stimulation with norepinephrine under normoxic conditions.