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• W2208366558 startingPage "H2658" @default.
• W2208366558 abstract "Physiological concentrations of [Arg 8 ]vasopressin (AVP; 10–500 pM) stimulate oscillations of cytosolic free Ca 2+ concentration (Ca 2+ spikes) in A7r5 vascular smooth muscle cells. We previously reported that this effect of AVP was blocked by a putative phospholipase A 2 (PLA 2 ) inhibitor, ONO-RS-082 (5 μM). In the present study, the products of PLA 2 , arachidonic acid (AA), and lysophospholipids were found to be ineffective in stimulating Ca 2+ spiking, and inhibitors of AA metabolism did not prevent AVP-stimulated Ca 2+ spiking. Thin layer chromatography was used to monitor the release of AA and phosphatidic acid (PA), which are the products of PLA 2 and phospholipase D (PLD), respectively. AVP (100 pM) stimulated both AA and PA formation, but only PA formation was inhibited by ONO-RS-082 (5 μM). Exogenous PLD (type VII; 2.5 U/ml) stimulated Ca 2+ spiking equivalent to the effect of 100 pM AVP. AVP stimulated transphosphatidylation of 1-butanol (a PLD-catalyzed reaction) but not 2-butanol, and 1-butanol (but not 2-butanol) completely prevented AVP-stimulated Ca 2+ spiking. Protein kinase C (PKC) inhibition, which completely prevents AVP-stimulated Ca 2+ spiking, did not inhibit AVP-stimulated phosphatidylbutanol formation. These results suggest that AVP-stimulated Ca 2+ spiking depends on activation of PLD rather than PLA 2 and that PKC activation may be downstream of PLD in the signaling cascade." @default.
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• W2208366558 date "2001-06-01" @default.
• W2208366558 modified "2023-10-17" @default.
• W2208366558 title "Vasopressin-stimulated Ca²⁺spiking in vascular smooth muscle cells involves phospholipase D" @default.
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• W2208366558 doi "https://doi.org/10.1152/ajpheart.2001.280.6.h2658" @default.
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