(Hypertension. 2002;40:448.)
© 2002 American Heart Association, Inc.
Editorial Commentary |
From the Center for Clinical Pharmacology, Departments of Medicine and Pharmacology, University of Pittsburgh Medical Center, Penn.
Correspondence to Edwin K. Jackson, Center for Clinical Pharmacology, University of Pittsburgh School of Medicine, 626 Scaife Hall, 3550 Terrace St, Pittsburgh, PA 15261. E-mail edj+@pitt.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Epidemiological studies demonstrate sexual dimorphism with respect to arterial blood pressure, incidence of vascular disease, and the rate of progression of renal disease. In this regard, in men age <60 years, arterial blood pressure is higher compared with that of age-matched women, and the incidence of coronary artery disease is 50% less in premenopausal women compared with age-matched men. Decline of kidney function in patients with chronic renal disease is slowed in premenopausal women compared with age-matched men.
After the loss of ovarian function, sexual dimorphisms vis-à-vis hypertension, vascular disease, and rate of progression of kidney disease are no longer present. Arterial blood pressure increases in postmenopausal women, and the incidence of vascular disease and the rate of progression of renal disease equalizes between men and women.
The association of loss of ovarian function and disappearance of sexual dimorphism with respect to hypertension and vascular and renal disease suggests that 17ß-estradiol, the major estrogen produced by the human ovary, may importantly participate in the relative protection afforded to premenopausal women. The conclusion that 17ß-estradiol protects against hypertension, vascular damage, and progression of renal disease is corroborated by animal studies demonstrating antihypertensive, vasculoprotective, and renoprotective effects of 17ß-estradiol.
Like 17ß-estradiol, inhibitors of the renin-angiotensin system, such as ACE inhibitors or angiotensin receptor blockers (ARBs), also reduce blood pressure, protect blood vessels against vascular injury, and have renoprotective effects. Whether these beneficial effects of inhibitors of the renin-angiotensin system are nonadditive, additive, or synergistic with 17ß-estradiol is a critically important question that
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