Published online before print December 6, 2004, doi: 10.1161/01.HYP.0000151825.36598.36
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(Hypertension. 2005;45:170.)
© 2005 American Heart Association, Inc.
Hypertension Highlights |
Sex Steroids, Cardiovascular Disease, and Hypertension
Unanswered Questions and Some Speculations
From the Department of Physiology and Biophysics and The Center for Excellence in Cardiovascular and Renal Research, University of Mississippi Medical Center, Jackson.
Correspondence to Jane F. Reckelhoff, Department of Physiology and Biophysics and The Center for Excellence in Cardiovascular and Renal Research, University of Mississippi Medical Center, 2500 N State St, Jackson, MS 39216. E-mail jreckelhoff@physiology.umsmed.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
The roles that both male and female sex steroids play in mediating or protecting against cardiovascular disease (CVD) and hypertension are controversial. For example, whereas animal studies have strongly implicated androgens as being mediators of CVD and hypertension, human epidemiological studies have shown that with chronic disease, including hypertension, serum testosterone levels are actually reduced.1 Thus, whether androgens are truly causative of CVD is not clear. However, premenopausal women are typically protected from CVD and hypertension compared with men, and this has been hypothesized to be because of the protective effects of estrogens. The negative findings of Heart and Estrogen/progestin Replacement Study (HERS) I and II2,3 and Women’s Health Initiative (WHI)4,5 studies on hormone replacement therapy (HRT) in postmenopausal women have shaken our previous ideas that HRT was protective against CVD. In this short review, the latest findings regarding the roles of sex steroids in hypertension and CVD are discussed, questions yet to be answered are suggested, and some speculations are made.
Sex Steroids and Receptors
In both males and females, the hypothalamus secretes gonadotropin-releasing hormone, which stimulates the anterior pituitary to release both luteinizing hormone and follicular-stimulating hormone. Luteinizing hormone binds to receptors on thecal cells in ovaries of females and Leydig cells in testes of males to cause testosterone to be synthesized. Follicular-stimulating hormone, however, binds to receptors on granulosa cells in females or Sertoli cells in males and stimulates the synthesis of aromatase, which converts testosterone to estradiol.
There are 2 main types of estrogen receptors, ER
and ERß, but several
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