CHANGES OF BLOOD-PRESSURE RESPONSIVENESS IN RATS EXPOSED IN-UTERO ANDPERINATALLY TO A HIGH-SALT ENVIRONMENT

We tested the hypothesis that the presser responses to angiotensin II could be influenced by an early salt exposure. Twenty-five adult femal e rats were pseudorandomly divided in two groups. Twelve animals under went a partial ligature of their abdominal aorta (PAL). Once polydipsi a and sodium appetite developed, these rats were mated. The other grou p (13 rats) was sham-operated (Sham) and mated. Throughout pregnancy a nd lactation, water and 2.7% NaCl solution intakes differed between th e two groups of mother rats. PAL offspring (PAL-O; n = 14), and Sham-o perated offspring (Sh-O; n = 10), were maintained on a solid diet cont aining 1% NaCl, tap water and a 2.7% NaCl solution. At 90 days of age, presser responsiveness to intravenous angiotensin II (50, 100 and 200 ng) was assessed in anesthetized rats. The presser responses to 50 an d 200 ng angiotensin II were significantly greater in PAL-O rats than in Sh-O rats. These results support the hypothesis of a modulation of cardiovascular responsiveness or its underlying mechanisms by an early high salt environment.