Influences of Panax notoginsenosid on spontaneous contraction of small intestine smooth muscle of rabbits in vitro.
- Author:
Qian LI
1
;
Yue GUAN
;
Hui-jie MA
;
Zan GUO
;
Rui-rong HE
;
Yi ZHANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Calcium; metabolism; Depression, Chemical; Drugs, Chinese Herbal; pharmacology; Female; In Vitro Techniques; Intestine, Small; physiology; Male; Muscle Contraction; drug effects; Muscle, Smooth; metabolism; physiology; Nitric Oxide; metabolism; Panax notoginseng; chemistry; Rabbits
- From: Chinese Journal of Applied Physiology 2010;26(1):117-120
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the influences of Panax notoginsenosid(a compound of Chinese Traditional Medicine) on the spontaneous contraction of small intestine smooth muscle of rabbits in vitro and explore the mechanism.
METHODSThe influences of Panax notoginsenosid on the spontaneous contraction of small intestine in intacted rabbits(male or female) after the isothermal perfuse of small intestine in vitro were observed. Bay K8644 and nitro-L-arginine methylester (L-NAME) were added to the normal Tyrode's solution respectively before Panax notoginsenosid. In the Ca2+ free Tyrode's solution, rynodine was added before Panax notoginsenosid. The mechanism of Panax notoginsenosid was studied.
RESULTSPanax notoginsenosid reduced the amplitude of contraction of small intestine smooth muscle in rabbits in a does-depended manner. Bay K8644 and L-NAME could completely block the inhibition of Panax notoginsenosid on the contraction of small intestine smooth muscle. Panax notoginsenosid inhibited significantly the intracellular calcium-depended contraction induced by rynodine in the Ca2+ free Tyrode's solution.
CONCLUSIONPanax notoginsenosid inhibits significantly the contraction of small intestine smooth muscle of rabbits in vitro. The mechanism may be related to increase NO concentration in small intestine smooth muscle so that inhibit extracellular Ca2+ inflowing via cell membrane and intracellular Ca2+ releasing via sarcoplasmic reticulum.