Effects of 3-morpholinosydnonimine-N-ethylcarbamide on hypoxia-induced mechanical and electric responses of isolated pig coronary artery
Abstract
AIM:
To study effects of 3-morpholinosydnonimine-N -ethylcarbamide (SIN-1) on hypoxia-induced mechanical and electric activities of the isolated pig coronary artery.
METHODS:
Mechanical tension and membrane potential were measured simultaneously.
RESULTS:
Hypoxia initially caused a transient vascular smooth muscle cell membrane hyperpolarization followed by a membrane depolarization in isolated pig coronary artery. Subsequent addition of SIN-1 100 mumol . L-1 or verapamil (Ver) 10 mumol . L-1 led to membrane repolarization and relaxation of the vascular smooth muscle. Nitro-L-arginine (NLA) 0.2 mmol . L-1 and KCI 40 mmol . L-1 also induced membrane depolarization and vasoconstriction, which were similarly suppressed by SIN-1 or Ver.
CONCLUSION:
Hypoxic contractile response in isolated pig coronary artery is mediated by an increased Ca2+ influx via suppression of nitric oxide release.
Keywords:
To study effects of 3-morpholinosydnonimine-N -ethylcarbamide (SIN-1) on hypoxia-induced mechanical and electric activities of the isolated pig coronary artery.
METHODS:
Mechanical tension and membrane potential were measured simultaneously.
RESULTS:
Hypoxia initially caused a transient vascular smooth muscle cell membrane hyperpolarization followed by a membrane depolarization in isolated pig coronary artery. Subsequent addition of SIN-1 100 mumol . L-1 or verapamil (Ver) 10 mumol . L-1 led to membrane repolarization and relaxation of the vascular smooth muscle. Nitro-L-arginine (NLA) 0.2 mmol . L-1 and KCI 40 mmol . L-1 also induced membrane depolarization and vasoconstriction, which were similarly suppressed by SIN-1 or Ver.
CONCLUSION:
Hypoxic contractile response in isolated pig coronary artery is mediated by an increased Ca2+ influx via suppression of nitric oxide release.