Effects of Estrogen and Progestogen Treatment on the Response of the Aorta of Male Rats to Hypertension: MORPHOLOGICAL AND CHEMICAL STUDIES

Abstract

The effects of estrogen and progestogen treatment on the response of the thoracic aortic wall of male rats to hypertension were studied. Hypertension levels induced by cupping the renal artery were similar in untreated (H), estrogen-treated (E), and progestogen-treated (P) hypertensive groups. Hypertension of 8 weeks' duration caused increased wall thickness, increased calculated tangential tension, and increased medial area in groups H and P compared to normotensive controls (C), but wall thickness and medial area in groups E and C were similar despite the striking elevation in calculated tension and wall stress in group E. Chemical studies also showed that the absolute amounts of aortic collagen and elastin in groups H and P were similarly increased over group C values, but absolute amounts of both these fibrous proteins in vessels from group E were no different from those of group C. Noncollagenous alkali-soluble proteins in these vessels were present in absolute and relative amounts corresponding to the following rank: P > H > E > C.Thus, it appears that estrogen-treatment has a distinctly inhibitory effect and progestogen-treatment a slightly stimulatory effect on the aortic wall response to hypertension. Since hypertension-induced morphological and chemical changes have many similarities to features of arteriosclerotic plaque growth, recognition of these differences in hormonal effects on the response of the vessel wall to hypertension may have implications beyond their physiological role as sex hormones.KEY WORDS female sex hormones vessel wall tension elastin collagen blood vessels arteriosclerosis vascular disease renal hypertension • Two prominent features of the developing arteriosclerotic plaque are proliferation of smooth muscle cells and accumulation of extracellular fibrous proteins (1, 2). The initiating causes of these changes have been speculated on at length but remain unproved. Hypertension, both spontaneous and experiFrom the

Analysis of Gender Difference of Cardiac Risk Biomarkers Using hGH-Transgenic Mice

“…In addition, the result that a significant increase in LPO was observed only in the transgenic males may be explained by the antioxidative effects of estrogen. It has also been reported that arteriosclerosis is inhibited by the antioxidative effects of estrogen [32], and endothelial cell-protective action [6]. These reported findings may account for why no significant effects of abnormal hGH secretion on cardiac and liver function were observed in the transgenic females in the present study.…”

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

“…Experiments in laboratory animals proved that oestrogens dilate the large arteries. 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.…”

“…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.…”

Effects of two forms of hypertension on atherosclerosis in the hyperlipidemic baboon.

“…50 It increases the extent of musculoelastic intimal plaques in rhesus monkeys, 51 increases medial wall thickness, 52 increases endothelial cell proliferation, 53 " 55 occasionally produces endothelial denudation, 58 stimulates intimal accumulation in the acute phase of hypertension but not in the chronic phase, 57 alters endothelial structure, 58 alters endothelial gap junctions, 59 increases aortic connective tissue, 40 and increases in vitro cholesterol biosynthesis. 60 Schwartz 61 compared the effects of hypertension and atherosclerosis on both endothelial and smooth muscle cell replication.…”