Effect of 17 Beta-estradiol on Delayed Outward Potassium Current
نویسندگان
چکیده
منابع مشابه
Effects of allocryptopine on outward potassium current and slow delayed rectifier potassium current in rabbit myocardium
OBJECTIVE Allocryptopine (ALL) is an effective alkaloid of Corydalis decumbens (Thunb.) Pers. Papaveraceae and has proved to be anti-arrhythmic. The purpose of our study is to investigate the effects of ALL on transmural repolarizing ionic ingredients of outward potassium current (I to) and slow delayed rectifier potassium current (I Ks). METHODS The monophasic action potential (MAP) techniqu...
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The purpose of this study was to determine the effects of 17-beta-estradiol on area postrema neuronal activity in vivo and on area postrema potassium currents (IK) in vitro. In anesthetized rats, intravenous injection of 17-beta-estradiol (10 ng/kg bw) -inhibited area postrema neuronal activity in 8/8 neurons tested. The averaged firing rate decreased from 2.9 +/- 1.1 to 1.1 +/- 0.3 Hz. The inh...
متن کاملTransient outward potassium current in ICC.
Interstitial cells of Cajal (ICC) are the pacemakers of the gut, initiating slow-wave activity. Several ion channels have been identified that contribute to the depolarization phase of the slow wave. Our aim was to contribute to knowledge about the identity and role of ICC potassium channels in pacemaking. Here we describe a transient outward potassium current in cell-attached patches of ICC. T...
متن کاملEffect of acidosis on transient outward potassium current in isolated rat ventricular myocytes.
The effect of acidosis on the transient outward K(+) current (I(to)) of rat ventricular myocytes has been investigated using the perforated patch-clamp technique. When the holding potential was -80 mV, depolarizing pulses to potentials positive to -20 mV activated I(to) in subepicardial cells but activated little I(to) in subendocardial cells. Exposure to an acid solution (pH 6.5) had no signif...
متن کاملEnhancement of outward potassium current may participate in beta-amyloid peptide-induced cortical neuronal death.
In light of recent evidence implicating the upregulation of outward K+ current in mediating several forms of neuronal apoptosis, we tested the hypothesis that such an upregulation might specifically contribute to the pathogenesis of beta-amyloid peptide (A beta)-induced neuronal death. Exposure to A beta fragment 25-35 (20 microM) or 1-42 (20 microM) enhanced the delayed rectifier K+ current IK...
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ژورنال
عنوان ژورنال: The Showa University Journal of Medical Sciences
سال: 2000
ISSN: 0915-6380,2185-0968
DOI: 10.15369/sujms1989.12.277