2006
DOI: 10.1016/j.ijcard.2005.06.033
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Selective inhibition of pinacidil effects by estrogen in guinea pig heart

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Cited by 6 publications
(5 citation statements)
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“…[36, 37] Antiarrhythmic drugs that prolong the QT interval increase risk for torsade-de-pointes in women and was the reason some such drugs were removed from the market. [38] Estrogenic compounds modulate potassium currents in atrial tissue [39, 40], but the relationship between endogenous and exogenous estrogen on incidence of AF in women is not established.…”
Section: The Heartmentioning
confidence: 99%
“…[36, 37] Antiarrhythmic drugs that prolong the QT interval increase risk for torsade-de-pointes in women and was the reason some such drugs were removed from the market. [38] Estrogenic compounds modulate potassium currents in atrial tissue [39, 40], but the relationship between endogenous and exogenous estrogen on incidence of AF in women is not established.…”
Section: The Heartmentioning
confidence: 99%
“…It has been suggested that estrogen changes the modulation of the sarcK ATP channel binding site for pinacidil. 39 If this is true for rat ventricular myocytes, estrogen may prevent the modulation of sarcK ATP channels in female rats that have been given pinacidil.…”
Section: The Effect Of K Atp Channel Modulators On I/r-induced Arrhythmias In Femalesmentioning
confidence: 99%
“…It could be explanation for recently demonstrated increase in mortality due to cardiovascular events in postmenopausal women treated by hormone replacement therapy [13]. Therefore, apart from recently published data about estrogen effects on the function of ATP-sensitive K + channels [24], here we presented additional data about an important action of estrogen on the β-adrenoceptors in the heart, which are crucial for the regulation of heart work during ischaemia.…”
Section: Discussionmentioning
confidence: 85%