Arginine vasopressin promotes transient contractile responses through distinct mechanisms in rat aorta and mesenteric resistant arteries

Abstract Purpose Neurohormone-regulated peripheral vascular resistance is considered one of the factors governing blood pressure. This study was designed to evaluate the effect of arginine vasopressin (AVP) on contraction of endothelium-intact or -denuded rat aorta and mesenteric resistant arteries. Methods The wire myograph technique was used to assess the contractility of the vascular smooth muscles in response to a high-K+, phenylephrine, AVP, and inhibitors, etc. The time-course of agonist-evoked contraction was then recorded. The endothelium of the mesenteric resistance arteries and abdominal aorta were denuded by physical abrasion, as evidenced by acetylcholine-induced vasodilation dysfunction. Results Our result revealed that (1) AVP, but neither high K+ nor phenylephrine, evoked transient contraction of abdominal aorta and mesenteric resistance arteries; (2) Endothelial removal, V2 receptor antagonists, sGC inhibitors, or nitric oxide(NO) synthase inhibitors reversed the transient contraction of mesenteric resistance arteries into sustained contraction, but not in aorta;(3) Pharmacological inhibition of GRK2 altered AVP-elicited temporal contractile response into a sustained contraction in denuded aortic endothelium;(4) The vasopressin receptor V1A blocker abolished AVP-induced contractile responses in both vessel preparations. Conclusion V2-mediated NO pathway in endothelium and the V1A-mediated GRK2 signaling pathways in smooth muscle are involved in AVP-induced transient contractions in rat mesenteric resistance and aortic vessels, respectively.