Gender Differences in the Vasomotor Effects of Different Steroid Hormones in Rat Pulmonary and Coronary Arteries

Abstract

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.

The Effects of Endogenous Sex Hormones and Acute Hypoxia on Vasoconstriction in Isolated Rat Pulmonary Artery Rings

“…These results are in contrast to the studies of English et al [13] and Wetzel et al [23,24]. Since the experiments by Wetzel et al were performed in isolated sheep lungs, it is conceivable that the discrepancy between those studies and our study may be due to the fact that different models and different species were investigated.…”

“…Therefore, it is possible that the exclusion of estrus, metestrus and diestrus females may unmask sex-hormone specific effects. However, neither the studies by Wetzel et al [23,24] and English et al [13] nor previous studies from our lab [2] took the menstrual cycle into account. Yet, these studies demonstrated gender differences.…”

“…Both testosterone and estrogen have been shown to acutely affect vasoreactivity in various vascular beds [11,12]. Acute administration of estrogen or testosterone to pulmonary arteries causes vasorelaxation under normoxic conditions [13]. Interestingly, pulmonary vasodilation was greater when testosterone was administered compared to estrogen [13].…”

Sex and Menopause Differences in Response to Tadalafil: 6‐Minute Walk Distance and Time to Clinical Worsening

“…17 This postmenopausal increase is also demonstrated in PAH and is postulated to be due to estrogen withdrawal, as it has been demonstrated in animal models that lower estrogen and progesterone states produce increased pulmonary vasoconstriction. 17,[21][22][23][24] Despite the known effects of estrogen on the pulmonary vasculature, it remains unclear how menopause affects response to treatment of PAH in general, including with phosphodiesterase type 5 (PDE-5) inhibitors. A treatment agent with a postmenopausal-specific treatment benefit would be extremely valuable given the high prev-alence of PAH in this population compared with that in men and younger women.…”

Cardiovascular Effects of Androgens

“…Androgens influence cardiac function by acting directly on the heart or by affecting the vascular system (English et al, 2001;Hayward et al, 2001;Jones et al, 2003;Kienitz & www.intechopen.com Quinkler, 2008). In humans and experimental animals, anabolic steroids have been associated with an increased risk of coronary artery disease by adversely affecting the plasma lipid and lipoprotein profile, producing thrombosis and cardiac hypertrophy Sullivan et al, 1998).…”