[Arg8]-vasopressin-induced responses on coronary and mesenteric arteries of rats with myocardial infarction: the effects of V1a- and V2-receptor antagonists.

After myocardial infarction, plasma levels of [Arg8]-vasopressin rise to recover hemodynamics. The vascular responses to [Arg8]-vasopressin were studied in vitro in isolated hearts and mesenteric artery segments of rats with 1-day and 3-week-old infarcts, in absence and presence of the V1a-receptor antagonist SR-49059 and the V2-receptor antagonist OPC-31260. Vascular responses of coronary arteries were similar in sham and infarcted hearts. On average, coronary flow was maximally decreased by 70 +/- 3% from baseline values of 11.1 +/- 0.3 ml/min, with pD2 values of 10.52 +/- 0.05. In mesenteric artery segments of sham and infarcted rats, maximal contractile forces, expressed as percentage of contraction to 125 mM KCl, were similar (232 +/- 23% and 239 +/- 8%, respectively). However, pD2 values from infarcted rats (9.22 +/- 0.07) were significantly lower compared with sham (9.55 +/- 0.07) rats. In coronary as well as mesenteric vessels, the vasoconstrictor responses, being more susceptible to SR-49059 (apparent pA2, between 9.12 and 9.82) than to OPC-31260 (apparent pA2, between 6.21 and 6.92), seemed mediated by the V1a receptor. These data indicate that in mesenteric but not in coronary vessels, an altered responsiveness to vasopressin could be observed. Responses are mediated mainly by the V1a receptor.

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