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Inositol phospholipids localized to caveolae in rat heart are regulated by ₁-adrenergic receptors and by ischemia-reperfusion

Cellular Biochemistry Laboratory, Baker Heart Research Institute, Melbourne, Victoria, Australia

Submitted 16 November 2005 ; accepted in final form 20 December 2005

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 ₁-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. Caveolar fractions were prepared by buoyant density sucrose gradient centrifugation. [³H]PIP₂ was concentrated in caveolae, along with Gq and PLC1b. Caveolae contained only 27.3 ± 6.9% (means ± SE, n = 6) of the total ₁-adrenergic receptor complement of the heart. These did not migrate to PIP₂-containing caveolar fractions with norepinephrine stimulation under normoxic conditions, even though caveolar PIP₂ was depleted. In contrast, [³H]PIP₂ in caveolae increased during 2 min of reperfusion, independently of norepinephrine release and thus of ₁-adrenergic receptor activation. The increased PIP₂ in the caveolar fractions where signaling proteins are concentrated may be critical for the heightened generation of Ins(1,4,5)P₃ in early reperfusion.

lipid signaling; light lipid rafts; phospholipase C; Gq; caveolin

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