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Am J Physiol Regul Integr Comp Physiol (September 30, 2004). doi:10.1152/ajpregu.00309.2004
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Submitted on May 11, 2004
Accepted on September 20, 2004

Postnatal Modulation of Prenatally Programmed Hypertension by Dietary Na and ACE Inhibition

Jennifer Manning1 and V. Matti Vehaskari1*

1 Department of Pediatrics, Louisiana State University Health Sciences Center, The Research Institute for Children, New Orleans, LA, USA

* To whom correspondence should be addressed. E-mail: vvehas{at}lsuhsc.edu.

Adult hypertension in the rat can be programmed experimentally by changes in intrauterine environment. The offspring typically do not become hypertensive until 6 to 8 weeks of age, and recent evidence suggests that renal dysfunction may participate in the pathogenesis. The present study was based on the hypothesis that the window for programming extends to the postnatal period in the rat. Adult hypertension was induced by maternal low protein diet during the second half of gestation. After weaning at 3 weeks, the offspring were exposed to one of the following regimens for the subsequent 3 weeks: 1) low Na diet, 2) standard Na diet, 3) high Na diet, and 4) standard Na diet with enalapril. The pups were followed for 10 weeks after discontinuation of the treatments. The brief exposure to low Na diet or enalapril totally prevented the development of hypertension and the effect lasted throughout the observation period. The development of hyperreninemia, present in the standard Na group at 16 weeks of age, was abolished in the low Na and enalapril groups. Conversely, 3-week exposure to high Na diet increased the severity of the later hypertension and did not prevent the hyperreninemia. The findings suggest that there is a period of susceptibility during which prenatally programmed hypertension can be modulated postnatally, possibly coinciding with a critical stage in renal maturation.




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