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1 The Research Institute for Children, New Orleans, LA, USA; Department of Pediatrics, Louisiana State University Health Sciences Center, New Orleans, LA, USA
2 Department of Pediatrics, Louisiana State University Health Sciences Center, New Orleans, LA, USA
3 Department of Physiology, Tulane University Health Sciences Center, New Orleans, LA, USA
* To whom correspondence should be addressed. E-mail: vvehas{at}lsuhsc.edu.
Adult hypertension may be programmed by prenatal environment in humans and in experimental animals. The potential role of intrarenal renin-angiotensin system (RAS) in prenatally programmed hypertension was investigated. Hypertension in rat offspring was induced by maternal protein restriction during pregnancy. The offspring were studied on day 1 of life and immediately preceding the development of hypertension, on day 28. Angiotensin I and II contents were determined by radioimmunoassy. Angiotensin receptor protein and mRNA levels were quantified by immunoblotting and real-time RT-PCR, respectively. Plasma and kidney angiotensin I and II were unchanged in the offspring from low protein pregnancies (LP). Angiotensin II type 1 receptor (AT1R) protein abundance was low in the newborn LP kidney (P<0.05) but rose above control values by 28 days of age (P<0.05); the rise was associated with an increase in AT1R subtype A (P<0.01), but not subtype B, mRNA level. Angiotensin II type 2 receptor protein expression was decreased on day 1 (P<0.05) and increased on day 28 (P<0.05) in LP kidneys. The results show that prenatal programming of hypertension is associated with an abnormal pattern of intrarenal RAS ontogeny which may play a pathogenetic role, for instance by constitutively altering renal hemodynamics or Na reabsorption.
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