Mazumder P K, Gupta A K, Kumar D, Dube S N
Defence Research and Development Establishment, Gwalior.
Indian J Physiol Pharmacol. 1997 Jul;41(3):257-62.
Calcium modulatory activity of a marine toxin has been studied employing in vitro preparations. The toxin induced contracture in rat diaphragm was not modified by denervation, d-tubocurarine and tetrodotoxin (TTX). In contrast, varying concentrations of calcium, EGTA and ryanodine inhibited the contracture significantly. The toxin produced a series of repeating contractions in vas deferens. Experiments with TTX, adrenoceptor blockers and other agents exclude a release of neuromediators or direct stimulation of post synaptic receptors to account for the rhythmic effect in vas deferens. The dependence of rhythmicity on external Ca2+ concentration and inhibiting effect of Mn2+, ryanodine and nifedipine indicate a direct activation of voltage-sensitive calcium channel. The toxin also evoked a similar pattern of response in paced atria mediated through Ca2+ influx.
已利用体外制剂研究了一种海洋毒素的钙调节活性。该毒素诱导的大鼠膈肌挛缩不受去神经、d -筒箭毒碱和河豚毒素(TTX)的影响。相反,不同浓度的钙、乙二醇双(2 -氨基乙基醚)四乙酸(EGTA)和兰尼碱可显著抑制挛缩。该毒素在输精管中产生一系列重复收缩。用TTX、肾上腺素能受体阻滞剂和其他药剂进行的实验排除了神经介质释放或对突触后受体的直接刺激以解释输精管中的节律性效应。节律性对细胞外Ca2 +浓度的依赖性以及锰离子、兰尼碱和硝苯地平的抑制作用表明电压敏感性钙通道被直接激活。该毒素还通过Ca2 +内流在起搏心房中诱发了类似的反应模式。