RATS WITH HYPERTENSION INDUCED BY IN-UTERO EXPOSURE TO MATERNAL LOW-PROTEIN DIETS FAIL TO INCREASE BLOOD-PRESSURE IN RESPONSE TO A HIGH-SALT INTAKE

Citation
Sc. Langleyevans et Aa. Jackson, RATS WITH HYPERTENSION INDUCED BY IN-UTERO EXPOSURE TO MATERNAL LOW-PROTEIN DIETS FAIL TO INCREASE BLOOD-PRESSURE IN RESPONSE TO A HIGH-SALT INTAKE, Annals of nutrition & metabolism, 40(1), 1996, pp. 1-9
Citations number
39
Categorie Soggetti
Nutrition & Dietetics","Endocrynology & Metabolism
ISSN journal
02506807
Volume
40
Issue
1
Year of publication
1996
Pages
1 - 9
Database
ISI
SICI code
0250-6807(1996)40:1<1:RWHIBI>2.0.ZU;2-Q
Abstract
Hypertension in the rat has been demonstrated to be determined in uter o by exposure to maternal low-protein diets. Assessment was made of th e response of rats with maternal diet-induced hypertension to a chroni c high intake of sodium chloride. Normotensive and hypertensive animal s were provided with either drinking water (control) or 1.5% sodium ch loride over a 7-day period. Normotensive rats significantly increased blood pressure in response to the increased salt intake. 5-7 days afte r the start of the study systolic blood pressure was 30-41 mm Hg highe r than in controls. 7 days of salt drinking did not alter blood pressu re in maternal low-protein diet-exposed, hypertensive rats. In both no rmotensive and hypertensive groups provision of 1.5% sodium chloride s ignificantly increased fluid intake. In hypertensive rats the increase d fluid intake appeared to be an immediate response, whilst normotensi ve rats increased intake only after the first day. Urinary volume was increased in both groups of animals receiving salt, within 1 day, and Na+ excretion similarly increased by between 3.5- and 4.5-fold in both groups. K+ excretion initially decreased significantly in both normot ensive and hypertensive rats drinking 1.5% sodium chloride, but return ed to pre-salt drinking levels by day 5 of the experiment. Rats with m aternal-diet-induced hypertension appear to be insensitive to the hype rtensive effects of sodium chloride. This insensitivity does not appea r to stem from a more rapid clearance of excess sodium, and may relate to other aspects of kidney function and metabolism.