title: Effect of a perinatal high-salt diet on blood pressure control mechanisms in young Sprague-Dawley rats.
abstract: 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 [high-salt (HS) rats] 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 diet (NS rats). In HS rats, mean arterial pressure (MAP) was significantly increased (110 +/- 5 vs. 96 +/- 3 mmHg) compared with NS rats. Blockade of brain AT(1) receptors with intracerebroventricular losartan decreased MAP in HS but not NS rats. Blockade of alpha-adrenergic receptors with intravenous phentolamine or ganglionic transmission with intravenous 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 of (125)I-[Sa (1),Ile(8)]ANG II to AT(1) receptors was increased in the subfornical organ (SFO) of the HS rats. Expression of AT(1a) 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 AT(1) receptor activation.
authors.affiliation: Department of Physiology and Developmental Biology, Brigham Young University, Provo, UT 84602, USA.
authors.forename: Steven J
authors.initials: SJ
authors.lastname: Swenson
authors.forename: Robert C
authors.initials: RC
authors.lastname: Speth
authors.forename: James P
authors.initials: JP
authors.lastname: Porter
mesh_terms: D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000804:Angiotensin II / Q000378:metabolism; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000008:administration & dosage / Q000494:pharmacology; D000818:Animals; D000831:Animals, Newborn / Q000502:physiology*; D000959:Antihypertensive Agents / Q000008:administration & dosage / Q000494:pharmacology; D017704:Baroreflex / Q000187:drug effects; D001794:Blood Pressure / Q000187:drug effects*; D005260:Female; D005730:Ganglionic Blockers / Q000494:pharmacology; D006339:Heart Rate / Q000187:drug effects; D017403:In Situ Hybridization; D007276:Injections, Intraventricular; D019808:Losartan / Q000008:administration & dosage / Q000494:pharmacology; D011247:Pregnancy; D051381:Rats; D017207:Rats, Sprague-Dawley; D012083:Renin / Q000097:blood; D017673:Sodium Chloride, Dietary / Q000494:pharmacology*; D013356:Subfornical Organ / Q000187:drug effects / Q000378:metabolism; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000254:growth & development
chemical_list: D000317:Adrenergic alpha-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D000959:Antihypertensive Agents; D005730:Ganglionic Blockers; D017673:Sodium Chloride, Dietary; D000804:Angiotensin II; D012083:Renin; D019808:Losartan