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CHLORIDE ION INGESTED WITH SODIUM AFFECTS THE DEVELOPMENT OF CEREBRAL LESIONS IN STROKE‐PRONE SPONTANEOUSLY HYPERTENSIVE RATS
Author(s) -
Ikeda K.,
Nara Y.,
Yamori Y.
Publication year - 1991
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 - 10.1111/j.1440-1681.1991.tb01469.x
Subject(s) - sodium , calcium , medicine , endocrinology , chemistry , urine , homeostasis , chloride , stroke (engine) , mechanical engineering , organic chemistry , engineering
SUMMARY 1. To determine the effect of chloride ion on the development of hypertension and the incidence of cerebral lesions in stroke‐prone spontaneously hypertensive rats (SHRSP), groups of 10 rats were administered chronically with either 171 mmol/L sodium chloride or equimolar sodium provided as sodium citrate in the drinking water from the age of 12 weeks. 2. The life span was significantly extended in SHRSP given sodium citrate (336 ± 28 vs 246 ± 26 days, mean ± s.e.m., P <0.05) but their development of hypertension was not different from SHRSP given sodium chloride. 3. In order to determine the role of calcium homeostasis, calcium in urine was collected. Urinary calcium in SHRSP given sodium citrate was significantly decreased (1.0 ± 0.12 vs 1.8 ± 0.18 mg/ 24 h urine, P <0.05). 4. If the normal life span is 320 ± 35 days, this suggests that chloride ion ingested with sodium accelerates the development of cerebrovascular diseases, and that increased urinary calcium excretion may be related to this adverse chloride effect on the development of hypertension in SHRSP.