Lack of effect of a selective vasopressin V_1A receptor antagonist, SR 49,059, on potentiation by vasopressin of adrenoceptor‐mediated pressor responses in the rat mesenteric arterial bed

Abstract

1 The vasopressin receptor subtype involved in the enhancement by vasopressin of adrenoceptormediated vasoconstriction was investigated in rat isolated perfused mesenteric arteries. 6 In arteries precontracted with methoxamine (7.5 mM) pressor responses to [Arg 8 ]vasopressin (3 ± 10 nM) were not inhibited by a dose of SR 49,059 (3 nM) which abolished the peptide's vasoconstrictor e ect under control conditions. 7 These data show that the direct vasoconstrictor e ect of [Arg 8 ]vasopressin is mediated by V 1A receptors while the enhancement of adrenoceptor-mediated pressor responses is insensitive to V 1A , V 1B , and oxytocin receptor antagonists and is not mimicked by selective agonists of V 1B and V 2 receptors. In conclusion, an unusual interaction of vasopressin with V 1A receptors, or even the existence of a novel receptor subtype, has to be considered.

Prolactin‐Releasing Peptide Regulates the Cardiovascular System Via Corticotrophin‐Releasing Hormone

“…AVP, the nonselective V1 A/B and oxytocin receptor antagonist [deamino‐Pen 1 , Tyr (Me) 2 , Arg 8 ], and vasopressin (V1‐R antagonist) were obtained from Sigma (St Louis, MO, USA). The doses of AVP and the antagonist were 2 pmol and 0.4 nmol, respectively (27, 28). CRH and a nonselective antagonist, α‐helical CRH (9‐41), were obtained from Sigma and Peptide Institute, Inc. (Osaka, Japan), respectively.…”