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(Hypertension. 2008;51:997.)
© 2008 American Heart Association, Inc.

Go Red Editorial Commentaries

Sex, Salt, and Senescence

Sorting Out Mechanisms of the Developmental Origins of Hypertension

Jeffrey S. Gilbert

From the Department of Physiology and Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson, Miss.

Correspondence to Jeffrey S. Gilbert, Department of Physiology and Biophysics, University of Mississippi Medical Center, 2500 N State St, Jackson, MS 39216-4505. E-mail jsgilbert@physiology.umsmed.edu

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

The developmental origins of health and disease hypothesis derives from clinical observations indicating long-term health consequences, such as hypertension, for persons of low birth weight.¹ Considering that the kidneys hold such a prominent role in the long-term control of blood pressure, it is not surprising that subsequent observations from human and animal studies have found associations between nephron deficit (of fetal origin) and adult hypertension, although these observations have not been without controversy.¹ Numerous experimental models have been developed that support this hypothesis and seek to elucidate the mechanisms by which perinatal stressors affect fetal development to generate persistent elevations in the blood pressure of the offspring and of the subsequent hypertension during later life.^1–4 Throughout this body of work investigating the developmental origins of hypertension and regardless of the type of experimental insult, several common themes have emerged: the necessary involvement of the kidney,^1–5 dysregulation of the renin-angiotensin system (RAS),^1–3,5 and gender differences in response to the various stimuli.^1,2,5

Although it has long been observed that a variety of endocrine and nutritional insults during renal development result in developmental deficits in the kidney (reviewed elsewhere¹⁾, abnormalities in the RAS appear to be a central common pathway.⁶ The importance of the intrarenal RAS in renal development has been recognized for over a decade, when initial studies, such as those by Friberg et al,⁷ recognized that angiotensin II type 1 (AT₁) receptor antagonism during nephrogenesis leads to development deficits in the kidney. Hence, experimental studies using AT₁ receptor antagonism . . . [Full Text of this Article]

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