It is well recognised that oestrogens possess vasodilatory properties, and similar responses to testosterone have been demonstrated. However, vasomotor effects of other steroid hormones have not been well described. Direct comparisons of the relative vasoactivity of different steroid hormones in different vascular beds in male and female genders have not been made. Coronary and pulmonary arteries from adult Wistar rats were mounted in a wire myograph, loaded to 100 and 17 mmHg respectively, maximally pre-contracted with 1 x 10(-4) M prostaglandin-F-2-alpha, and dose response curves to 1 x 10(-6) to 1 x 10(-3) or 3 x 10(-3) M of 17 beta-oestradiol, testosterone, progesterone, and cortisol dissolved in water were constructed. Addition of each steroid hormone caused acute, dose dependent dilatation in coronary and pulmonary vessels. In coronary arteries the order of activity was testosterone > progesterone > 17 beta-oestradiol > cortisol, p < 0.001. In pulmonary arteries, the order of activity was progesterone > testosterone > cortisol > 17 beta-oestradiol, p < 0.001. Pulmonary arteries from male animals were more sensitive to the effects of testosterone than those from female animals, p = 0.003, whereas coronary arteries from female animals were more sensitive to the effects of 17 beta-oestradiol than those from male animals, p < 0.001. We have demonstrated significant differences in the in vitro vasomotor effects of different steroid hormones in two distinct vascular beds. Gender differences in vasomotor responses to steroid hormones may play a role in the aetiology of vasospastic diseases.

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T acts as a vasodilator in vitro and in vivo. Supplemental T therapy in humans with angina improves symptoms and reduces objective measures of ischemia. In left anterior descending coronary arteries taken from adult male Wistar rats, T abolishes 100+/-4.2% of calcium-dependent contraction induced by potassium chloride, 82.3+/-6.1% of the mostly calcium-dependent contraction induced by prostaglandin-F-2-alpha, but only 45.3+/-3.4% of the contraction induced by phorbol-12,13-dibutyrate (PDBu) in the presence of extracellular calcium, and 54.5+/-4.5% of the contraction induced by PDBu in the absence of extracellular calcium. These findings suggest that T is primarily inhibiting the calcium-dependent elements of vascular contraction.