Article date: March 1997
By: Koji Fujii, Uran Onaka, Yusuke Ohya, Susumu Ohmori, Mitsuhiro Tominaga, Isao Abe, Yutaka Takata, Masatoshi Fujishima, in Volume 120, Issue 7, pages 1207-1214
The role of eicosanoids in altered membrane electrical properties of Dahl salt‐sensitive (DS) rats was investigated, by use of conventional microelectrodes technique, in isolated superior mesenteric arteries of DS rats and Dahl salt‐resistant (DR) rats fed either a high or low salt diet.
The membrane was significantly depolarized in salt‐loaded DS rats compared with the other three groups. In addition, the arteries of salt‐loaded DS rats exhibited spontaneous electrical activity.
Spontaneous electrical activity in salt‐loaded DS rats was inhibited by the following: indomethacin, a cyclo‐oxygenase inhibitor; ONO‐3708, a prostaglandin H2/thromboxane A2 receptor antagonist; OKY‐046, a thromboxane A2 synthase inhibitor; nicardipine, a Ca2+‐channel antagonist and by Ca2+‐free solution. In addition, spontaneous electrical activity was enhanced by a thromboxane A2 analogue and by prostaglandin H2. Spontaneous electrical activity was unaffected by phentolamine, atropine and tetrodotoxin.
Membrane potential in arteries of salt‐loaded DS rats was not affected by either indomethacin or ONO‐3708.
Spontaneous contraction, sensitive to indomethacin, was present, and contractile sensitivity to high potassium solution was enhanced in arteries of salt‐loaded DS rats.
These findings suggest that eicosanoid action, together with membrane depolarization, may lead to the activation of voltage‐dependent Ca2+‐channels, thereby causing spontaneous electrical activity in mesenteric arteries of salt‐loaded DS rats. In addition, tension data suggest that these changes in membrane properties are related to enhanced contractile activities in salt‐loaded DS rats. Mechanisms of depolarization remain to be determined.
The role of eicosanoids in altered membrane electrical properties of Dahl salt‐sensitive (DS) rats was investigated, by use of conventional microelectrodes technique, in isolated superior mesenteric arteries of DS rats and Dahl salt‐resistant (DR) rats fed either a high or low salt diet.
The membrane was significantly depolarized in salt‐loaded DS rats compared with the other three groups. In addition, the arteries of salt‐loaded DS rats exhibited spontaneous electrical activity.
Spontaneous electrical activity in salt‐loaded DS rats was inhibited by the following: indomethacin, a cyclo‐oxygenase inhibitor; ONO‐3708, a prostaglandin H2/thromboxane A2 receptor antagonist; OKY‐046, a thromboxane A2 synthase inhibitor; nicardipine, a Ca2+‐channel antagonist and by Ca2+‐free solution. In addition, spontaneous electrical activity was enhanced by a thromboxane A2 analogue and by prostaglandin H2. Spontaneous electrical activity was unaffected by phentolamine, atropine and tetrodotoxin.
Membrane potential in arteries of salt‐loaded DS rats was not affected by either indomethacin or ONO‐3708.
Spontaneous contraction, sensitive to indomethacin, was present, and contractile sensitivity to high potassium solution was enhanced in arteries of salt‐loaded DS rats.
These findings suggest that eicosanoid action, together with membrane depolarization, may lead to the activation of voltage‐dependent Ca2+‐channels, thereby causing spontaneous electrical activity in mesenteric arteries of salt‐loaded DS rats. In addition, tension data suggest that these changes in membrane properties are related to enhanced contractile activities in salt‐loaded DS rats. Mechanisms of depolarization remain to be determined.
British Journal of Pharmacology (1997) 120, 1207–1214; doi:10.1038/sj.bjp.0701023
DOI: 10.1038/sj.bjp.0701023
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