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Either sodium deprivation or sodium excess sensitizes angiotensin (ANG) II‐induced hypertension
Author(s) -
Xue Baojian,
Zhang Zhongming,
Beltz Terry,
Guo Fang,
Johnson Alan Kim
Publication year - 2013
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.27.1_supplement.695.12
Subject(s) - sodium , endocrinology , medicine , renin–angiotensin system , angiotensin ii , aldosterone , blood pressure , chemistry , dietary sodium , high sodium , organic chemistry
Dietary sodium is known to regulate renin‐angiotensin‐aldosterone system (RAAS) activity, in which sodium deprivation activates the circulating RAAS, while sodium excess suppresses activity in that system. However, a recent study showed that the activity of RAAS was either not suppressed or, even augmented, after 4 weeks of salt loading despite high salt intake and increased blood pressure (BP). Our previous studies using an Induction‐Delay‐Expression (I‐D‐E) experimental design have demonstrated that one‐week ANG II pretreatment can sensitize the brain to produce an enhanced hypertensive response to subsequent ANG II. The present study tested the hypothesis that changes in dietary sodium (deficit or excess) can sensitize the pressor actions of ANG II. Three groups of male rats were implanted for telemetered BP recording and were maintained on 1) normal rat chow, 2) sodium‐deficient diet or 3) chow with 2% NaCl for two weeks, respectively. Then all groups were treated with subcutaneous ANG II (120 ng/kg/min) and normal chow for 2 weeks. Under both conditions where dietary sodium was manipulated, the animals responded with enhanced hypertension to ANG II (sodium deprivation 36.0±6.9 mmHg, high salt 34.8±4.1 mmHg, normal diet 19.6±3.8 mmHg). The results indicate that either sodium deprivation or sodium excess can sensitize the development of ANG II‐induced hypertension.