Original Article

Inhibition of beta-estradiol on trachea smooth muscle contraction in vitro and in vivo.

Authors: Jin-Jiang PANG, Xiang-Bin XU, Hong-Fang LI, Xiao-Yu ZHANG, Tian-Zhen ZHENG, Song-Yi QU

Abstract

AIM: To investigate the effect of beta-estradiol on trachea smooth muscle
contraction in vitro and in vivo.
METHODS: (1) Rabbit tracheas were incubated in organ baths filled with Krebs
solution and supplied with a mixed gas of 95 % O2 and 5 % CO2. The isometric
force was measured by ink-writing recorders. (2) The incubation period of asthma
induced by histamine and acetylcholine (ACh) in guinea pig were measured before
and after beta-estradiol (1 mg/kg) were given intramuscularly.
RESULTS: (1) Administration of beta-estradiol (0.1 mmol/L) caused relaxation of
isolated trachea muscle strips (TMS) in rabbits pre-contracted by ACh and KCl (39
% +/- 5 % and 45 % +/- 19 %). The presence of indomethacin or methylene blue
partly decreased the relaxation to beta-estradiol (26 % +/- 8 % and 28 % +/- 13
%), but Nomega-nitro-L-arginine (L-NNA) and propranolol and epithelium removal
did not affect it (38 % +/- 10 %, 40 % +/- 15 %, 37 % +/- 8 %). beta-Estradiol
can shifted the concentration-response curves of ACh and CaCl2 to the rightward
(pD2 = 3.98 and 4.75). In addition, it could also significantly inhibit the
contraction of phase caused by ACh, but did not affect the contraction of phase
II caused by CaCl2. (2) The incubation period of asthma in guinea pig were
delayed by beta-estradiol (1 mg/kg) given intramuscularly.
CONCLUSION: (1) The relaxation of beta-estradiol in vitro was epithelium
independent and associated with the inhibition of potential-dependent channel and
release of Ca2+ from sarcoplasm reticulum induced by ACh. In addition, release of
prostaglandins from trachea smooth muscle cells and relaxation through cGMP
approach were also included. beta-Adrenoceptor-mediated relaxation was not
involved. (2) beta-Estradiol can relax the trachea in vivo in guniea pig.
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