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Different Effects of Estrogen and Progesterone on K + Currents Expressed in Xenopus Oocytes
Author(s) -
Wong CM,
Yao XQ,
Tsang SY,
Huang Y
Publication year - 2002
Publication title -
journal of cardiac surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.428
H-Index - 58
eISSN - 1540-8191
pISSN - 0886-0440
DOI - 10.1046/j.1540-8191.2002.101419.x
Subject(s) - xenopus , estrogen , medicine , potassium channel , endocrinology , tetraethylammonium , hormone , chemistry , potassium , biochemistry , gene , organic chemistry
Potassium channel plays an active role in the regulation of membrane potential in vascular smooth muscle and vascular tone. These channels not only participate in the physiological responses to endogenously occurring substances, but also become the therapeutic targets for many synthetic drugs. Information regarding the role of K + channels in vascular effects of female sex steroid hormones is scarce. We previously showed that K + channel activation contributed in part to the estrogen‐mediated vasorelaxation. In order to examine further whether steroid hormones may have direct interaction with K + channels, we have recently expressed two types of K + channels, K Ca and K V channels in Xenopus oocytes. It was found that 17ß‐estradiol increased the large‐conductance K Ca currents in a concentration‐related manner. Tetraethylammonium ions or iberiotoxin inhibited the effect of 17ß‐estradiol. K Ca current was increased by NS 1619 and inhibited by progesterone. BSA‐conjugated estrogen also increased K Ca currents. Progesterone reduced the estrogen‐stimulated K Ca currents. K V1.5 channels were also expressed in Xenopus oocytes and inhibited by 4‐aminopyridine. Progesterone reduced the K V1.5 current, while estrogen had little effect. These results showed that estrogen could stimulate K Ca channels without an effect on K V1.5 channels. Progesterone inhibited the activity of both K Ca and K V1.5 channels expressed in Xenopus oocytes. Progesterone was described to antagonize the vascular action of estrogen. Inhibition of K + channels may be involved in the reported antagonistic effect of progesterone against the estrogen‐induced vasorelaxation. (supported by UPGC Direct Grant)