J Menopausal Med.  2014 Apr;20(1):1-6.

Postmenopausal Hypertension and Sodium Sensitivity

Affiliations
  • 1Department of Urology, Soonchunhyang University, College of Medicine, Bucheon, Korea.
  • 2Department of Obstetrics and Gynecology, Soonchunhyang University, College of Medicine, Bucheon, Korea.
  • 3Department of Nephrology, Yale University, School of Medicine, New Haven, USA.
  • 4Department of Cellular and Molecular Physiology, Yale University, School of Medicine, New Haven, USA. tong.wang@yale.edu

Abstract

It has been well established that women generally have lower incidence rates of hypertension than men at similar ages and these differences may vary with age. It also has been observed in many studies that after menopause, blood pressure (BP) increases in women to levels even higher than in men. The lack of estrogens may not be suggested as the only component involved in the development of postmenopausal hypertension. Thus, in this mini-review, the possible mechanisms by which sex hormones may influence the BP are discussed. This review also examines the renal regulatory mechanisms for gender differences in BP and explores the effects of salt intake on BP (salt-sensitivity) in pre and post-menopausal women. Estrogen has been shown to stimulate nitric oxide (NO) production, thus female sex hormones have a beneficial effect on BP control. Evidences that angiotensin type 2 receptor (AT2R) is up-regulated by estrogen support the favorable effects on BPs in women than men. The kidney plays an integral role in the regulation of arterial pressure through the mechanism of pressure-natriuresis, which has been shown to be modulated by the RAS. The prevalence of salt-sensitivity increases with age and low-salt diets has shown to help reduce systolic BP (SBP) and diastolic BP. While oral hormone replacement therapy has yielded only a neutral or minimal effect on the elevation of SBP, both the transdermal route replacement and a novel progestin with anti-aldosterone activity (drospirenone) has also shown to reduce SBP.

Keyword

Blood pressure; Gender difference; Hypertension; Postmenopause; Sodium excretion

MeSH Terms

Arterial Pressure
Blood Pressure
Diet, Sodium-Restricted
Estrogens
Female
Gonadal Steroid Hormones
Hormone Replacement Therapy
Humans
Hypertension*
Incidence
Kidney
Male
Menopause
Nitric Oxide
Postmenopause
Prevalence
Receptor, Angiotensin, Type 2
Sodium*
Estrogens
Gonadal Steroid Hormones
Nitric Oxide
Receptor, Angiotensin, Type 2
Sodium

Figure

  • Fig. 1 (A) Renal major regulatory mechanism of blood pressure (BP) and sodium excretion. Increased BP induces sodium excretion via pressure-natriuresis relationship, and angiotensin II (Ang II) and nitric oxide (NO) modulate this relationship. Female and male sex hormones affect this process via the regulation of renin- Ang II and NO. (B) Pressure-natriuresis relationship. If it shifts rightward, the amount of sodium excretion will decrease in the same mean arterial pressure. (ECF: extracellular fluid, BP: blood pressure)

  • Fig. 2 Different renal response between salt-sensitive and salt-resistant subjects. Glomerular filtration rate is maintained after salt loading in salt-resistant subjects. The rate decreases in salt-senitive subjects. (GFR, glomerular filtration rate)


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