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Short‐Term Incubation with Physiological Level of Estrogen Impairs ß 1 ‐Adrenoceptor‐Mediated but Enhances ß 2 ‐Adrenoceptor Mediated Coronary Relaxation
Author(s) -
Chan HY,
Yao XQ,
He GW,
Tsang SY,
Wong CM,
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.1540-8191.2002.101416.x
Subject(s) - endocrinology , medicine , estrogen , agonist , incubation , phenylephrine , estrogen receptor , adrenergic , adrenergic receptor , receptor , chemistry , blood pressure , biochemistry , cancer , breast cancer
Considerable evidence suggests that ß‐adrenoceptors are subject to regulation by sex steroid hormones. It was reported that estrogen replacement potentiated the vascular responses mediated by ß‐adrenoceptor activation by an endothelium‐independent mechanism. ß‐Adrenoceptor is present on both vascular smooth‐muscle and endothelial cells. However, no experiment has examined the effect of acute exposure to physiological concentrations of estrogen on ß‐adrenoceptor–mediated vasorelaxation in mammalian arteries. The major observation in this study is that the relaxant response to ß 2 ‐adrenoceptor activation with fenoterol was significantly enhanced by short‐term incubation (1 hr) with 0.3 nM 17ß‐estradiol in the isolated porcine coronary circumflex arteries. This effect was abolished by pretreatment with 10‐μM tamoxifen. Preincubation with 17ß‐estradiol (0.3 nM) reduced the relaxant response to dobutamine, a ß 1 ‐adrenoceptor agonist. The concentration of 0.3 nM falls into the reported circulating level of estrogen ranging between 0.1 and 1 nM in the body. Low concentrations of estrogen appeared to slightly enhance the relaxation induced by isoproterenol, a non‐selective ß‐ (ß 1 and ß 2 ) adrenoceptor agonist, following 1‐hr incubation. Physiological level of estrogen did not influence the relaxation induced by IBMX, an inhibitor of phosphodiesterase. In contrast, 20‐min exposure to 17ß‐estradiol (0.1–1 nM) was without effect on ß 1 ‐ or ß 2 ‐adrenoceptor‐mediated vascular responses. Our data indicate that acute exposure to physiological concentration of estrogen has differential effect on ß‐adrenoceptor‐mediated relaxation in porcine coronary arteries, increasing ß 2 ‐adrenergic response but decreasing ß 1 ‐adrenergic response. It would therefore be not surprising to observe a marginal effect of estrogen on relaxation induced by isoproterenol, an agonist that activates both ß 1 and ß 2 ‐adrenoceptors in blood vessels. (supported by UPGC Direct Grant)