Cardiovascular effects of arginine vasotocin in the rainbow trout Oncorhynchus mykiss

Abstract

The physiological functions of the neurohypophyseal hormone arginine vasotocin (AVT) in teleosts are not clear. In the present studies, the sites and mechanisms of action of AVT on the rainbow trout Oncorhynchus mykiss cardiovascular system were examined in unanesthetized instrumented fish, perfused organs and isolated vessels. Injection of AVT (1, 10 or 100 pmol kg-1 body mass) into trout with dorsal aortic cannulas produced a modest, but dose-dependent, increase in dorsal aortic pressure (P(DA)). Bolus injection of AVT (100 pmolkg-1body mass), or continuous infusion (6.7 pmol kg-1 min-1), into trout instrumented with dorsal aortic, ventral aortic and central venous cannulas and a ventral aortic flow probe significantly increased PDA as well as ventral aortic (P(VA)) and central venous (P(VEN)) blood pressure. Bradycardia accompanied the rapid rise in P(VA) while gill resistance (R(G)) increased. Maximum response to the AVT bolus was reached within 13-21 min and the response decayed slowly over the ensuing 90 min. AVT infusion (6.7 pmolkg-1min-1) significantly increased P(VEN) and mean circulatory filling pressure and decreased unstressed blood volume, whereas venous compliance was unaffected. These in vivo studies indicate that AVT increases venous tone, thereby mobilizing blood from the unstressed compartment into the stressed compartment. This increases P(VEN), which increases venous return and helps maintain, or slightly elevate, cardiac output. This, combined with an elevated R(G) and slightly elevated systemic resistance (R(S)), increases both P(VA) and P(DA); however, the rise in P(DA) is mitigated by a disproportionate increase in R(G) relative to R(S). In vitro, the effects of AVT are consistent with in vivo responses. AVT increased vascular resistance in the perfused gill and perfused trunk and contracted isolated vascular rings from both rainbow and steelhead trout. The general order of sensitivity of isolated vessels to AVT was (in decreasing order): anterior cardinal vein, celiacomesenteric artery, ductus Cuvier, efferent branchial artery, ventral aorta and coronary artery. Extracellular Ca2+ accounted for over 70 % of the tension in the AVT-contracted efferent branchial artery, but only 57 % of the tension in the anterior cardinal vein. Vascular AVT receptor sensitivity (EC50) in vitro ranged from 0.3 to 6 nmol l-1 and was similar to the estimated ED50 for the dose-dependent increase in P(DA) in vivo (approximately 1 nmol l-1). AVT was not inotropic in paced ventricular rings nor did it exhibit vasorelaxant activity in perfused organs or vascular rings. These results show that AVT is a potent vasoconstrictor in trout and that its two primary cardiovascular targets are the systemic veins and the branchial vasculature.