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Interactions Between Sodium And Angiotensin
Author(s) -
Morgan Trefor
Publication year - 2001
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1046/j.1440-1681.2001.03577.x
Subject(s) - medicine , losartan , endocrinology , angiotensin ii , renin–angiotensin system , sodium , blood pressure , low sodium , blockade , high sodium , natriuresis , chemistry , receptor , organic chemistry
SUMMARY 1. Increased sodium intake causes decreased formation of angiotensin (Ang) II and increased AngII causes increased Na + retention. 2. Increased sodium intake and increased AngII causes cardiac hypertrophy, but decreased sodium intake regresses cardiac hypertrophy despite high AngII levels. Likewise, decreased Na + and blockers of the renin–angiotensin system (RAS) in neonatal rats have similar effects on subsequent blood pressure development. 3. Cardiac hypertrophy due to renal hypertension does not regress when the RAS is blocked and rats are on a high salt intake. Likewise, sodium restriction alone does not cause regression; combination of reduced NaCl intake and RAS blockade is required. 4. High doses of perindopril and losartan in combination cause a syndrome in rats on 0.2% NaCl that leads to profound hypotension, polyuria, renal impairment and involution of the heart and death. This is reversed or prevented by a high (4%) NaCl intake, which also prevents the plasma angiotensinogen depletion that occurs with combined blockade on 0.2% NaCl intake. 5. Intake of NaCl and AngII interact at many levels. It is postulated that there is an important interaction at the cellular level that can explain the above events.