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(Hypertension. 2008;52:615.)
© 2008 American Heart Association, Inc.

Editorial Commentaries

Why Can’t a Woman Be More Like a Man?

Is the Angiotensin Type 2 Receptor to Blame or to Thank?

Kathryn Sandberg; Hong Ji

From the Center for the Study of Sex Differences in Health, Aging, and Disease, Georgetown University, Washington, DC.

Correspondence to Kathryn Sandberg, Suite 232 Building D, Georgetown University, 4000 Reservoir Rd, NW, Washington, DC 20057. E-mail sandberg@georgetown.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

In Pygmalion, Henry Higgins asked, "Why can’t a woman be more like a man?" But when it comes to hypertension, Henry actually should have asked, "Why can’t a man be more like a woman?" Women have lower blood pressure (BP) and a lower incidence of hypertension than aged-matched men through much of their lives.¹ We need to understand why, because a better understanding of what protects the female from this potentially devastating disease ultimately could lead to new therapeutic treatments for both men and women. According to the American Heart Association, hypertension is a disease that afflicts >73 million people and kills >50 000 people per year in the United States alone. Uncontrolled hypertension leads to heart failure, myocardial infarction, stroke, and renal failure. Surprisingly, we still do not know the cause of essential hypertension, although it accounts for >90% of all cases of hypertension.

In this issue of Hypertension, using a model of angiotensin II (Ang II)–induced hypertension, Sampson et al¹ suggest that the angiotensin type 2 receptor (AT₂R) provides a major clue for solving the mystery of sex differences in hypertension. Ang II infusion is a widely used experimental model of hypertension, because inhibitors of Ang II synthesis and action have been very effective clinically to treat hypertension. In fact, most hypertensive patients respond to Ang II synthesis inhibitors and angiotensin type 1 receptor (AT₁R) blockers, indicating that essential hypertension is primarily Ang II dependent. Thus, the mechanisms uncovered in this experimental model are . . . [Full Text of this Article]

Related Article:

Enhanced Angiotensin II Type 2 Receptor Mechanisms Mediate Decreases in Arterial Pressure Attributable to Chronic Low-Dose Angiotensin II in Female Rats

Amanda K. Sampson, Karen M. Moritz, Emma S. Jones, Rebecca L. Flower, Robert E. Widdop, and Kate M. Denton
Hypertension 2008 52: 666-671. [Abstract] [Full Text] [PDF]

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				D. J. Campbell Can the Study of Female Rats Help Our Understanding of Women? Hypertension, December 1, 2008; 52(6): e142 - e142. [Full Text] [PDF]