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1 Physiology and Developmental Biology, Brigham Young University, Provo, UT, USA
2 Pharmacology, University of Mississippi, University, MS, USA
* To whom correspondence should be addressed. E-mail: james_porter{at}byu.edu.
In the present investigation we sought to determine if a perinatal high-salt treatment affects blood pressure at an early age (30 days), and if so, to determine the mechanisms responsible for the hypertension. Pregnant dams were given an 8% NaCl diet (HS) during the final one third of gestation and throughout the suckling period. After weaning, the pups continued to receive the high-salt diet until testing at age 30 days. Control groups received a normal-salt (NS) diet. In HS rats, mean arterial pressure (MAP) was significantly increased (110 ± 5 versus 96 ± 3 mm Hg) compared to NS rats. Blockade of brain AT1 receptors with i.c.v. losartan decreased MAP in HS, but not NS rats. Blockade of 
-adrenergic receptors with i.v. phentolamine or ganglionic transmission with i.v. chlorisondamine produced a greater decrease in MAP in HS rats. Baroreflex control of heart rate was assessed using a four parameter logistics function. The mid-range MAP (p3) was significantly increased in the HS rats. No other baroreflex parameters were affected. Specific binding of125I-Sar1, Ile8 angiotensin II to AT1 receptors was increased in the subfornical organ (SFO) of the HS rats. Expression of AT1a receptor mRNA was greater in both SFO and PVN of the HS rats. These data suggest that even at an early age, Sprague Dawley rats treated with a perinatal high-salt diet are hypertensive. The elevated blood pressure appears to be caused by increased sympathetic nervous activity resulting, in part, from increased brain AT1 receptor activation.
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