期刊
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
卷 287, 期 2, 页码 F262-F267出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajprenal.00055.2004
关键词
fetal origins of adult disease; kidney ontogeny; low-protein diet
资金
- NHLBI NIH HHS [1 R01-HL-66158] Funding Source: Medline
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 RTPCR, respectively. Plasma and kidney ANG I and II were unchanged in the offspring from low-protein pregnancies ( LP). ANG II type 1 receptor (AT(1)R) 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 AT(1)R 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.
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