Modulation of Eicosanoid-Induced Contraction of Mouse and Rat Blood Vessels by Gingerols

The effects of the active principles of crude ginger (a traditional Sino-Japanese medicine), the gingerols, on the contractile responses to eicosanoids were compared using isolated mouse and rat blood vessels. Leukotrienes (LT) C4 and D4, a thromboxane (TX) A2 derivative (U-46619), prostaglandins (P...

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Bibliographic Details
Published in:Japanese Journal of Pharmacology 1989, Vol.50(3), pp.253-261
Main Authors: KIMURA, Ikuko, KIMURA, Masayasu, PANCHO, Leonora Rivera
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
blood vessels
Cardiovascular system
Catechols
Dinoprost - pharmacology
Drug Interactions
eicosanoids
Fatty Alcohols - pharmacology
In Vitro Techniques
Leukotrienes - pharmacology
Male
Medical sciences
Mice
Miscellaneous
Muscle Contraction - drug effects
Muscle, Smooth, Vascular - drug effects
Norepinephrine - pharmacology
Pharmacology. Drug treatments
Phenylephrine - pharmacology
Prostaglandins - pharmacology
Rats
Rats, Inbred Strains
smooth muscle
Splanchnic Circulation - drug effects
Zingiber officinale
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Summary:The effects of the active principles of crude ginger (a traditional Sino-Japanese medicine), the gingerols, on the contractile responses to eicosanoids were compared using isolated mouse and rat blood vessels. Leukotrienes (LT) C4 and D4, a thromboxane (TX) A2 derivative (U-46619), prostaglandins (PG) F2α, PG12-Na, PGE2, the stable PGI2 derivative TRK-100, and PGD2 induced contraction in longitudinal segments of mouse mesenteric veins in that order of potency. Exogenous arachidonic acid and PGE1, did not cause contraction. The mesenteric veins also contracted in response to noradrenaline (NA) and phenylephrine (PhE), but not to clonidine. The gingerols alone relaxed the muscle transiently and then augmented the response to PGF2α, PGE2, PGI2-Na, and TRK-100, but suppressed the response to PGD2, U-46619, LTC4, LTD4, NA and PhE. (±)-[6]-Gingerol also potentiated the PGF2α-induced contraction in longitudinal segments of rat mesenteric vein and vena cava, but inhibited it in circular segments of rat aorta and longitudinal segments of mouse mesenteric arteries. These results showed that (±)-[6]- and (±)-[8]-gingerols potentiated the contraction induced by prostanoids (except PGD2) and inhibited that produced by PGD2, TXA2, and LT, suggesting the modulation of eicosanoids-induced responses by (±)-[6]- or (±)-[8]-gingerol.
ISSN:0021-5198
1347-3506
DOI:10.1254/jjp.50.253