Role of AVP in maintenance of circulatory homeostasis during hemorrhagic shock

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Abstract
Hemorrhagic hypotension produces significantly increased plasma arginine vasopressin (AVP) concentrations. A specific antagonist (AVP-A, [1-.beta.-mercapto-.beta.,.beta.-cyclopentamethylenepropionic acid, 2-(O-methyl)tyrosine]) of the pressor effects of endogenous AVP was used to investigate the role of this neurohypophyseal hormone on the pathogenesis of hemorrhagic shock. Infusion of the AVP-A (2 .mu.g/kg bolus + 2 .mu.g .cntdot. kg-1 .cntdot. h-1 infusion) into sham-shocked animals produced no significant changes in any of the observed experimental variables. Cats subjected to hemorrhagic shock given AVP-A had final superior mesenteric artery flow (SMAF) values significantly (P < 0.05) higher than shock cats given vehicle (7.7 .+-. 1.1 vs. 4.5 .+-. 0.8 ml .cntdot. kg-1 .cntdot. min-1, respectively). Increases in postreinfusion plasma cathepsin D activities were significantly blunted in hemorrhaged animals treated with AVP-A (10.4 .+-. 2.0 vs. 24.8 .+-. 5.5 U/mg protein; P < 0.05). Plasma proteolysis as well as the plasma accumulation of myocardial depressant factor (MDF) were also significantly modulated by AVP-A treatment n hemorahed animals. MDF activities were 75 .+-. 6 and 53 .+-. 4 U/ml (P < 0.02) for shock cats given vehicle or AVP-A, respectively. These beneficial actions were not reflected in any significant improvement in postreinfusion mean arterial blood pressure (MABP). Apparently, endogenous AVP functions not only as a potent splanchnic vasoconstrictor but also a key humoral factor in the maintenance of postreinfusion MABP, a profile that is different from the role of angiotensin II, the other major splanchnic vasoconstrictor, in shock.