
Contractile Effects of Jellyfish Toxin Extracted from Carybdea rastonii on Isolated Rabbit Aorta
Author(s) -
Hiroshi Ozaki,
Hideaki Karaki,
Hajime Nagase,
Norimoto Urakawa,
Hiroshi Azuma,
Terumi Nakajima
Publication year - 1986
Publication title -
japanese journal of pharmacology/japanese journal of pharmacology
Language(s) - English
Resource type - Journals
eISSN - 1347-3506
pISSN - 0021-5198
DOI - 10.1254/jjp.42.425
Subject(s) - contraction (grammar) , bay k8644 , papaverine , nicardipine , phentolamine , chemistry , muscle contraction , contractility , trifluoperazine , medicine , vascular smooth muscle , endocrinology , aorta , anatomy , calcium , biophysics , biology , smooth muscle , nifedipine , propranolol , calmodulin
Effects of the toxic component of jellyfish (Carybdea rastonii) (pCrTX) on the smooth muscle tension of isolated rabbit thoracic aorta were examined. pCrTX, at concentrations higher than 10(-7) g/ml, caused slowly developing tension that reached its maximum after about 1 hr. This contraction was partially inhibited by pretreatment of the tissue with phentolamine (5 X 10(-6) M) or indomethacin (10(-5) M). The contraction induced by pCrTX was partially inhibited by nicardipine (10(-7) M) and markedly augmented by Bay k8644 (10(-6) M). In low-Na+ solution, the rate of rise of the pCrTX-induced contraction was significantly reduced. Removal of external Ca2+ inhibited the pCrTX-induced contraction by about 30%, while chlorpromazine, trifluoperazine, prenylamine and papaverine (10(-4) M) completely inhibited the contraction. pCrTX itself did not cause any contraction in saponin-skinned smooth muscle and had no effect on the Ca2+-induced contractile tension. It has been reported that pCrTX-induced contraction is attributable to the release of endogenous catecholamines and also to the increase in Ca2+ influx in smooth muscle (Azuma et al., 1986). The present results confirmed the previous suggestion and further suggested that a portion of the contraction is due to release of prostaglandin(s) and also to the direct effect on smooth muscle which is not dependent on Ca2+ influx.