V1a vasopressin-induced accumulation of inositol trisphosphate in cultured rat aortic myocytes; modulation by protein kinase C.
Arginine vasopressin stimulated the accumulation of labeled inositol phosphate in cultured rat aortic myocytes prelabeled with tritiated myo-inositol. This accumulation was prevented by pretreating the myocytes with the phorbol ester PMA. The time-course and concentration-effect curves were similar for inositol phosphate formation in myocytes and contractile effects on isolated aorta. Vasopressin agonists also stimulated inositol phosphate formation, whereas vasopressin-induced response could be inhibited by V1a-specific antagonists. These results suggest that stimulation of inositol phosphate formation in myocytes is due to V1a receptor activation and could be modulated by protein-kinase-C-mediated mechanisms.
D000818:Animals; D002478:Cells, Cultured; D015544:Inositol 1,4,5-Trisphosphate; D007295:Inositol Phosphates / Q000378:metabolism*; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000378:metabolism*; D011493:Protein Kinase C / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D013403:Sugar Phosphates / Q000378:metabolism*; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D014661:Vasoconstriction / Q000187:drug effects; D014667:Vasopressins / Q000494:pharmacology*
D007295:Inositol Phosphates; D013403:Sugar Phosphates; D014667:Vasopressins; D015544:Inositol 1,4,5-Trisphosphate; D011493:Protein Kinase C; D013755:Tetradecanoylphorbol Acetate