Hyperpolarization caused by serotonin contributes to endothelium-dependentrelaxations in the porcine coronary artery

Citation
Sj. Park et al., Hyperpolarization caused by serotonin contributes to endothelium-dependentrelaxations in the porcine coronary artery, ACT PHAR SI, 20(12), 1999, pp. 1093-1097
Citations number
11
Categorie Soggetti
Pharmacology & Toxicology
Journal title
ACTA PHARMACOLOGICA SINICA
ISSN journal
02539756 → ACNP
Volume
20
Issue
12
Year of publication
1999
Pages
1093 - 1097
Database
ISI
SICI code
0253-9756(199912)20:12<1093:HCBSCT>2.0.ZU;2-V
Abstract
AIM: The present study was designed to investigate the contribution of memb rane hyperpolarization Ito endothelium-dependent relaxations induced by ser otonin in the porcine coronary artery, METHODS: Rings with and without endo thelium of porcine coronary arteries were suspended in conventional organ c hambers for the measurement of isometric force. The cell membrane potential of the vascular smooth muscle cells was measured using glass microelectrod es, in the presence of indometacin, ketanserin, and/or N-omega-nitro-L-argi nine. RESULTS: Serotonin induced a transient endothelium-, and concentratio n-dependent relaxation in rings contracted with prostaglandin F-2 alpha in the presence of N-omega-nitro-L-arginine (maximal relaxation: 19 %). The N- omega-nitro-L-arginine resistant relaxation was abolished by high K+ and te trabutylammonium chloride. Serotonin also caused an endothelium-, concentra tion-dependent membrane hyperpolarizations with a maximal amplitude of -8.8 mV. The nitro-L-arginine resistant relaxations and hyperpolarizations were abolished by methiothepin, but not by glibenclamide. The time course of th e endothelium-dependent relaxations and hyperpolarizations was similar. CON CLUSION: These results suggest a contribution of cell membrane hyperpolariz ation to the endothelium-dependent relaxations induced by serotonin in the porcine coronary artery.