Mechanism of Acetylcholine-induced Endothelium-dependent Relaxation in the Rabbit Carotid Artery by M3-receptor Activation.
- Author:
Yong Jin SONG
1
;
Seong Chun KWON
Author Information
1. Department of Otolaryngology, Head & Neck Surgery, Kangnung Asan Hospital, Kangnung 210-711, Korea.
- Publication Type:Original Article
- Keywords:
Acetylcholine;
Vasorelaxation;
Nitric oxide;
Rabbit carotid artery
- MeSH:
Acetylcholine;
Arteries;
Atropine;
Carotid Arteries*;
Cytosol;
Endothelial Cells;
Endothelium;
Fura-2;
Gadolinium;
Lanthanum;
Muscle Tonus;
Nitric Oxide;
Nitroarginine;
Relaxation*;
Vasodilation
- From:The Korean Journal of Physiology and Pharmacology
2004;8(6):313-317
- CountryRepublic of Korea
- Language:English
-
Abstract:
The present study were designed to characterize the action mechanisms of acetylcholine (ACh) -induced endothelium-dependent relaxation in arteries precontracted with high K (70 mM). For this, we simultaneously measured both muscle tension and cytosolic free Ca2 concentration ([Ca2 ]i), using fura-2, in endothelium-intact, rabbit carotid arterial strips. In the artery with endothelium, high K increased both [Ca2 ]i and muscle tension whereas ACh (10microM) significantly relaxed the muscle and increased [Ca2 ]i. In the presence of NG-nitro-L-arginine (L-NAME, 0.1 mM), ACh increased [Ca2 ]i without relaxing the muscle. In the artery without endothelium, high K increased both [Ca2 ]i and muscle tension although ACh was ineffective. 4-DAMP (10 nM) or atropine (0.1microM) abolished ACh-induced increase in [Ca2 ]i and relaxation. The increase of [Ca2 ]i and vasorelaxation by ACh was siginificantly reduced by either 3microM gadolinium, 10microM lanthanum, or by 10microM SKF 96365. These results suggest that in rabbit carotid artery, ACh-evoked relaxation of 70 mM K -induced contractions appears to be mediated by the release of NO. ACh-evoked vasorelaxation is mediated via the M3 subtype, and activation of the M3 subtype is suggested to stimulate nonselective cation channels, leading to increase of [Ca2 ]i in endothelial cells.
