Contractile responses to histamine, serotonin, and angiotensin II are impaired by 17 beta-estradiol in human internal mammary arteries in vitro.

There is accumulating evidence that estrogen replacement therapy protects against the development of coronary atherosclerosis and myocardial infarction in postmenopausal women. The mechanism of this protective effect is uncertain. The purpose of the present study was to determine whether 17 beta-estradiol acutely modifies vascular smooth muscle contractile responses to various agonists in human arteries in vitro. Human mammary artery rings were obtained during aortocoronary bypass operations. Rings were suspended in organ baths for isometric tension measurements. Concentration response curves induced by serotonin (0.01-30 mumol/l), histamine (0.01-300 mumol/l), and angiotensin II (0.1-100 nmol/l) were generated after pre-incubation for 30 min with either 17 beta-estradiol (3 mumol/l) or solvent (0.2% ethanol). The presence of 17 beta-estradiol significantly reduced the maximal contractile effects induced by histamine, serotonin, and angiotensin II, but not by 80 mmol/l potassium chloride. It is concluded that short-term incubation with 17 beta-estradiol reduces the maximal contractile responses to serotonin, histamine, and angiotensin II. These modulating effects of estrogen on vascular tone may contribute to the proposed beneficial role of estrogen replacement therapy on the incidence of myocardial infarction in postmenopausal women.