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Cardiovascular pharmacology of 3‐ n ‐butylphthalide in spontaneously hypertensive rats
Author(s) -
Tsi D.,
Tan B. K. H.
Publication year - 1997
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/(sici)1099-1573(199712)11:8<576::aid-ptr174>3.0.co;2-7
Subject(s) - phenylephrine , nitric oxide , pharmacology , chemistry , nitric oxide synthase , caffeine , endothelium , endocrinology , lipid peroxidation , medicine , blood pressure , oxidative stress
The hypotensive and vasorelaxant effects of 3‐ n ‐butylphthalide (BuPh) and its possible mechanisms of action were investigated in spontaneously hypertensive rats (SHR) for the first time. A 13‐day intraperitoneal infusion of BuPh at doses of 2.0 and 4.0 mg/day produced a transient hypotensive effect while a dose of 0.5 mg/day showed a significant hypotensive effect only on day 12. BuPh at 0.5 mg/day had no effect on the plasma and tissue angiotensin converting enzyme (ACE) activities, or on the tissue lipid peroxidation index. BuPh relaxed endothelium‐intact and denuded aortic rings precontracted with phenylephrine and KCl. N G ‐nitro‐ L ‐arginine methyl ester, an inhibitor of nitric oxide synthase, did not attenuate the vasorelaxant activity of BuPh. The cumulative concentration response curves of phenylephrine and Ca 2+ (in CaCl 2 ‐free, high KCl medium) were non‐competitively inhibited by BuPh. However, BuPh did not interfere with the caffeine‐induced release of intracellular Ca 2+ . It appears that the vasorelaxant effect of BuPh could be attributed to the blockade of Ca 2+ entry, possibly through voltage‐ and receptor‐operated Ca 2+ channels, thereby lowering the systolic blood pressure of SHR. © 1997 John Wiley & Sons, Ltd.