Abstract
Coronary heart disease (CHD) is a major cause of mortality in First World countries in both men and women. Men exhibit up to a tenfold greater risk of CHD than women of premenopausal age. In women undergoing natural [1] or surgical menopause [2], the risk of CHD increases and approaches that of men. Cessation of ovarian function and loss of endogenous sex hormone production has been suggested to be the primary cause of the increase in risk of CHD observed in postmenopausal women. Indeed, hormone replacement therapy (HRT) studies have indicated that hormone replacement is associated with a reduction in both morbidity and mortality of around 50% [3]. This discrepancy in risk of CHD between the genders has prompted intense research into the vascular effects of female sex hormones. Studies on coronary occlusion as assessed by selective coronary arteriography have revealed that HRT users had a relative risk of coronary artery disease of 0.37–0.44 compared to non-users [4]. The female sex hormones, in particular estrogen, are believed to cause their relative cardioprotection in part by alterations in plasma lipoprotein levels [5]. Estrogens are able to increase plasma high density lipoproteins (HDL) while lowering low density lipoproteins (LDL) [6]. Given the positive association of the latter with CHD risk and the association of the former with cardiovascular protection, it was at first believed that this was the primary mechanism by which female sex hormones mediated cardiovascular benefit. However, studies quantifying the relative contribution of these changes to cardioprotection, concluded that changes in lipid profiles at most accounted for only 25%–50% of the effect of female sex hormones [7].
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References
Colditz GA, Willett WC, Stampfer MJ, Rosner B, Speizer FE, Hennekens CH. Menopause and the risk of coronary heart disease in women. N Engl J Med 1987;316:1105–10.
Adams MR, Kaplan JR, Clarkson TB, Koritnik DR. Ovariectomy. Social status and atherosclerosis in cynomolgus monkeys. Arteriosclerosis 1985;5:192–200.
Grady D, Rubin SM, Petitti DB, et al. Hormone therapy to prevent disease and prolong life in postmenopausal women. Ann Intern Med 1992;117:1016–37.
Gruchow HW, Anderson AJ, Barboriak JJ, Sobocinski KA. Postmenopausal use of estrogen and occlusion of coronary arteries. Am Heart J 1988;115:954–63.
Stevenson JC. The metabolic and cardiovascular consequences of HRT. Br J Clin Pract 1995;49:87–90.
Sitruk-Ware R. Estrogen therapy during the menopause.Practical treatment recommendations. Drugs 1990;39:203–17.
Walsh BW, Schiff I, Rosner B, Greenberg L, Ravnikar V, Sacks FM. Effects of postmenopausal estrogen replacement on the concentration and metabolism of plasma lipoproteins. N Engl J Med 1991;325:1196–1204.
Horwitz KB, Horwitz LD. Canine vascular tissues are targets for androgens, estrogens, progestins, and glucocorticoids. J Clin Invest 1982;69:750–58.
Lin AL, McGill HC Jr, Shain SA. Hormone receptors of the baboon cardiovascular system: Biochemical characterization of aortic and myocardial cytoplasmic progesterone receptors. Circ Res 1982;50:610–16.
McGill H. Sex steroid hormone receptors in the cardiovascular system. Postgrad. Med April 1989;85(pt.2):64–68.
Huang PL, Huang Z, Mashimo H, et al. Hypertension in mice lacking the gene for endothelial nitric oxide synthase. Nature 1995;377:239–42.
Hayashi T, Fukuto JM, Ignarro LJ, Chaudhuri G. Basal release of nitric oxide from aortic rings is greater in female rabbits than in male rabbits: Implications for atherosclerosis. Proc Natl Acad Sci 1992;89:11259–63.
Hishikawa K, Nakaki T, Marumo T, Suzuki H, Kato R, Saruta T. Up-regulation of nitric oxide synthase by estradiol in human aortic endothelial cells. FEBS Lett 1995;360:291–93.
Wingrove CS, Stevenson JC. 17-β estradiol inhibits stimulated endothelin-1 release from human vascular endothelial cells. Eur J Endocrinol 1997;137:205–8.
Washburn SA, Honoré EK, Cline JM, et al. Effects of 17-α dihydroequilenin sulfate on atherosclerotic male and female rhesus monkeys. Am J Obstet Gynecol 1996;175:341–51.
Bobik A, Grooms A, Millar JA, Mitchell A, Grinpukel S. Growth factor activity of endothelin on vascular smooth muscle. Am J Physiol 1990;258:C408–C415.
de Nucci G, Thomas R, D’Orleans-Juste P, et al. Pressor effects of circulating endothelin are limited by its removal in the pulmonary circulation and by the release of prostacyclin and endothelium-derived relaxing factor. Proc Natl Acad Sci USA 1988;85:9797–9800.
Haak T, Jungmann E, Felber A, Hillmann U, Usadel KH. Increased plasma levels of endothelin in diabetic patients with hypertension. Am J Hypertens 1992;5:161–66.
Cody RJ, Haas GJ, Binkley PF, Capers Q, Kelley R. Plasma endothelin correlates with the extent of pulmonary hypertension in patients with chronic congestive heart failure. Circulation 1992;85:504–9.
Polderman KH, Stehouwer CD, van Kamp GJ, Dekker GA, Verheugt FW, Gooren LJ. Influence of sex hormones on plasma endothelin levels. Ann Intern Med 1993;118:429–32.
Ylikorkala O, Orpana A, Puolakka J, Pyorala T, Viinikka L. Postmenopausal hormonal replacement decreases plasma levels of endothelin-1. J Clin EndocrinolMetab 1995;80:3384–87.
Morey AK, Razandi M, Pedram A, Hu R-M, Prins BA, Levin ER. Oestrogen and progesterone inhibit the stimulated production of endothelin-1. Biochem J 1998;330:1097–1105.
Buikema H, Pinto YM, Rooks G, Grandjean JG, Schunkert H, van Gilst WH. The deletion polymorphism of the angiotensin-converting enzyme gene is related to phenotypic differences in human arteries. Eur Heart J 1996;17:787–94.
Schuster H, Wienker TF, Stremmler U, Noll B, Steinmetz A, Luft FC. An angiotensin-converting enzyme gene variant is associated with acute myocardial infarction in women but not in men. Am J Cardiol 1995;76:601–3.
Proudler AJ, Ahmed AI, Crook D, Fogelman I, Rymer JM, Stevenson JC. Hormone replacement therapy and serum angiotensin-converting-enzyme activity in postmenopausal women. Lancet 1995;346:89–90.
Irey NS, Manion WC, Taylor HB. Vascular lesions in women taking oral contraceptives. Arch Path 1970;89:1–8.
Irey NS, Norris HJ. Intimal vascular lesions associated with female reproductive steroids. Arch Pathol 1973;96:227–34.
Fischer GM. In vivo effects of estradiol on collagen and elastin dynamics in rat aorta. Endocrinol 1972;91:1227–32.
Wingrove CS, Garr ED, Godsland IF, Stevenson JC. 17-β oestradiol enhances release of matrix metalloproteinase-2 from human vascular smooth muscle cells. Biochim Biophys Acta 1998;1406:169–74.
Register TC, Adams MR, Golden DL, Clarkson TB. Conjugated equine estrogens alone, but not in combination with MPA, inhibit aortic connective tissue remodeling after plasma lipid lowering in female monkeys. Arterioscler Thromb Vasc Biol 1998;18:1164–71.
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© 1999 Kluwer Academic Publishers and Fondazione Giovanni Lorenzini
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Wingrove, C.S., Stevenson, J.C. (1999). Action of Specific Estrogens on Vascular Cells. In: Women’s Health and Menopause. Medical Science Symposia Series, vol 13. Springer, Dordrecht. https://doi.org/10.1007/978-0-585-37973-9_8
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DOI: https://doi.org/10.1007/978-0-585-37973-9_8
Publisher Name: Springer, Dordrecht
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