Objective: To investigate the effect of arginine vasopressin (AVP) on vascular reactivity and calcium sensitivity following hemorrhagic shock and their relationship to protein kinase C (PKC) isoforms.
Methods: With endothelium denuded superior mesenteric artery (SMA) rings procured from rats in hemorrhagic shock, the effects of AVP (5x10(-11), 5x10(-10) and 5x10(-9) mol/L) on contractile responses to norepinephrine (NE) and calcium sensitivity of SMA from hemorrhagic shock in rats and their relationship to alpha and Delta isoforms of PKC with isolated organ perfusion system were observed.
Results: AVP (5x10(-11), 5x10(-10) and 5x10(-9) mol/L) markedly restored the vascular reactivity and calcium sensitivity following hemorrhagic shock, converting the cumulative concentration-response curve of NE and Ca2+ shift to the left, and its maximum concentration force (Emax) was significantly increased (all P<0.01) in a concentration dependent manner. Significant statistical differences were observed between the AVP groups (all P<0.05). Go6976 (5x10(-6) mol/L) and Rottlerin (10(-5) mol/L),respectively as the specific PKC alpha and PKC Delta isoforms inhibitor, antagonized AVP (5x10(-10) mol/L)-induced increase in vascular reactivity and calcium sensitivity of SMA following hemorrhagic shock and inhibited AVP-induced shift to the left of cumulative concentration-response curve of NE and Ca2+, and the Emax was significantly decreased (P<0.05 or P<0.01).
Conclusion: AVP significantly restored the decreased vascular reactivity and calcium sensitivity of vascular smooth muscle following hemorrhagic shock, and its underlying mechanisms may be related to both alpha and Delta isoforms of PKC activation.