Hyperpolarization caused by serotonin contributes to endothelium-dependent relaxations in the porcine coronary artery.
Abstract
AIM:
The present study was designed to investigate the contribution of membrane hyperpolarization to endothelium-dependent relaxations induced by serotonin in the porcine coronary artery.
METHODS:
Rings with and without endothelium of porcine coronary arteries were suspended in conventional organ chambers for the measurement of isometric force. The cell membrane potential of the vascular smooth muscle cells was measured using glass microelectrodes, in the presence of indometacin, ketanserin, and/or N omega-nitro-L-arginine.
RESULTS:
Serotonin induced a transient endothelium-, and concentration-dependent relaxation in rings contracted with prostaglandin F2 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 tetrabutylammonium chloride. Serotonin also caused an endothelium-, concentration-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 the endothelium-dependent relaxations and hyperpolarizations was similar.
CONCLUSION:
These results suggest a contribution of cell membrane hyperpolarization to the endothelium-dependent relaxations induced by serotonin in the porcine coronary artery.
Keywords:
The present study was designed to investigate the contribution of membrane hyperpolarization to endothelium-dependent relaxations induced by serotonin in the porcine coronary artery.
METHODS:
Rings with and without endothelium of porcine coronary arteries were suspended in conventional organ chambers for the measurement of isometric force. The cell membrane potential of the vascular smooth muscle cells was measured using glass microelectrodes, in the presence of indometacin, ketanserin, and/or N omega-nitro-L-arginine.
RESULTS:
Serotonin induced a transient endothelium-, and concentration-dependent relaxation in rings contracted with prostaglandin F2 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 tetrabutylammonium chloride. Serotonin also caused an endothelium-, concentration-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 the endothelium-dependent relaxations and hyperpolarizations was similar.
CONCLUSION:
These results suggest a contribution of cell membrane hyperpolarization to the endothelium-dependent relaxations induced by serotonin in the porcine coronary artery.