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1The Research Institute for Children, New Orleans 70118; 2Department of Pediatrics, Louisiana State University Health Sciences Center, New Orleans 70112; and 3Department of Physiology, Tulane University Health Sciences Center, New Orleans, Louisiana 70112
Submitted 17 February 2004 ; accepted in final form 13 April 2004
Adult hypertension may be programmed by the prenatal environment in humans and in experimental animals. The potential role of the 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. ANG 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 ANG I and II were unchanged in the offspring from low-protein pregnancies (LP). ANG 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. ANG 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 that may play a pathogenetic role, for instance, by constitutively altering renal hemodynamics or Na reabsorption.
fetal origins of adult disease; kidney ontogeny; low-protein diet
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