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Angiotensin II (AII) Modulates Sodium Chloride (NaCl) Intake in Backcrossed Borderline Genetic Hypertension
Author(s) -
Bradshaw Timothy John,
Welch Katherine A,
Osborn Jeffrey L
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a515-d
Subject(s) - captopril , endocrinology , medicine , angiotensin ii , appetite , offspring , chemistry , sodium , blood pressure , angiotensin ii receptor type 1 , saline , renin–angiotensin system , ingestion , losartan , weaning , biology , pregnancy , organic chemistry , genetics
AII and the regulation of NaCl intake was evaluated in a back‐cross model of Brown Norway (BN) and Spontaneously Hypertensive Rat (SHR). Female SHR (Aoki‐Okamoto strain; Charles River Labs, Inc.) were crossed with normotensive BN rats. Hypertensive (HT) F1 offspring then were sib‐sib crossed to produce F2 experimental offspring. F2 rats were raised from weaning and maintained on either 4.0% (HS) or 0.8% (NS) NaCl chow. When allowed to self‐titrate their NaCl intake, HS rats ingested more NaCl than NS rats over 5 days (3.46 ± 0.90 mM vs 1.54 ± 0.86 mM NaCl; p< 0.05), yet both groups had similar mean arterial pressures (MAP) (134.3 ± 17.01 mmHg vs 139.8 ± 27.92 mmHg; p>0.05). Ingestion of HS may increase brain and/or hypothalamic angiotensin (AT 1 ) receptors. HS and NS rats were provided ad lib access to water, 2% saline, and NaCl free chow. Blood pressure (BP), NaCl and H 2 O intakes, and urine flow rates were measured during control, AII blockade with captopril, and recovery. Captopril increased HS and NS NaCl ingestion by similar amounts and eliminated the difference in salt appetite between HS and NS rats. BP was not changed in either group by captopril. Thus, SHR raised on HS have increased sodium appetite that may involve exaggerated brain AII responses via increased expression of AT 1 receptors.