Journal of Vascular Medicine & Surgery

Abstract

Arginine Vasopressin Promotes Transient Contractile Responses through Distinct Mechanisms in Rat Aorta and Mesenteric Resistant Arteries

Weizhong Zhu*, Aihua Yang, Yifeng Zhang, Yuhang Wang, Xiaojun Wang, Hairong Bao and Jun Ren

Background: 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.

Method: 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: The 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, soluble Guanylate Cyclase (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 G-Protein Coupled Receptor 2 (GPCR2) altered AVP-elicited temporal contractile response into a sustained contraction in denuded aortic endothelium; (4) The vasopressin receptor V_1A blocker abolished AVP-induced contractile responses in both vessel preparations.

Conclusion: V₂-mediated NO pathway in endothelium and the V_1A-mediated GRK2 signaling pathways in smooth muscle are involved in AVP-induced transient contractions in rat mesenteric resistance and aortic vessels, respectively.

Published Date: 2024-11-27; Received Date: 2024-10-25