Effect of sex hormones on blood pressure and vascular connective tissue in castrated and noncastrated male rats

Abstract

Aortic collagen and elastin were quantitated in three groups of castrated and two groups of noncastrated male rats treated by intramuscular injection for 3 wk with oil, testosterone, or estradiol. The greatest differences were found between the castrated rats receiving testosterone and those receiving estradiol, the estradiol-treated rats having significantly lower total collagen, percent collagen, total elastin, and collagen/elastin (C/E), and higher percent elastin than those rats receiving testosterone. In noncastrated rats, administration of estradiol resulted in significantly lower total collagen, percent collagen, total elastin, and C/E. Systolic blood pressure was highest in rats receiving testerone and lowest in rats receiving estradiol. It is concluded that 1) estradiol in the presence or absence of testosterone decreases total accumulation of vascular connective tissue and alters the proportions of collagen and elastin so that the vessel is more distensible, 2) testosterone has an opposite but less marked effect than estradiol on vascular connective tissue, and 3) estradiol and testosterone alter blood pressure in opposite directions in the male rat.

Hypertension in women

“…The rapid time course of the reduction in arterial compliance after cessation of hormone replacement therapy and of the increase in compliance after reinstituting hormone treatment is more consistent with a vasodilator mechanism than with structural remodelling of the vessel wall, which would be expected to be a more lengthy process. 45 These findings are consistent with the transient nature (ie therapy must be continuous for benefit to be maintained) of the vasoprotective effects of postmenopausal hormone replacement therapy. 46 A more recent study evaluated systemic arterial compliance in 109 postmenopausal women receiving hormone replacement therapy compared with 108 age-matched untreated controls.…”

Menopause and the characteristics of the large arteries in a population study

“…28,29 In peri-and postmenopausal women, [30][31][32] they widen the smaller resistance vessels 33 by mechanisms that include the protection of endothelial function, 31 the potentiation of nitric oxide release 30,32 and the modulation of sympathetic reactivity. 24,34 Oestrogens may also influence the viscoelastic properties of the arterial wall by changing the relative proportions of collagen and elastin, 35 by inhibition of smooth muscle cell proliferation, or by the prevention of atherosclerotic stiffening. 36 Menopause does not occur as a sudden event but as a continuous transition from a regular menstrual cycle to ovarian failure.…”

“…Initially, the sample had been stratified by sex and age (20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35)(36)(37)(38)(39)(40)(41)(42)(43)(44)(45)(46)(47)(48)(49)(50)(51)(52)(53)(54)(55)(56)(57)(58)(59), у60 years), in an attempt to recruit the same number of subjects in each stratum. Households were identified from population registries as persons who shared the same address.…”

Sex Differences in Abdominal Aortic Aneurysm: The Role of Sex Hormones

“…In 1970s, before the AAA experimental models, Fischer et al 56 found that rats receiving estradiol had a higher aortic elastin/collagen ratio than those receiving testosterone. More recently, sex differences in AAA have been studied in different animal models, which include the intraluminal infusion of elastase in rats 57 or mice, 58 angiotensin II (AngII) infusion in mice deficient in apolipoprotein E (Apoe À/À ), 59 and direct application of elastase at the anterior wall of the abdominal aorta in mice (Table III).…”