Kurahashi K, Fujiwara M
Can J Physiol Pharmacol. 1976 Aug;54(4):577-82. doi: 10.1139/y76-079.
In the isolated taenia caeci of guinea pigs excess potassium (10-30 mM) induced a phasic relaxation followed by a contraction. This phasic relaxation was unaffected by treatment with hexamethonium, phentolamine, propranolol and bretylium. However, relaxation induced by perivascular nerve stimulation was inhibited by all these agents but not by hexamethonium. Tetrodotoxin inhibited both forms of relaxation. Potassium-induced relaxation was not accompanied by [3H]noradrenaline release. Perivascular nerve stimulation caused release of [3H]noradrenaline and this was blocked by bretylium. Treatment with ouabain or replacement of NaCl by LiCl, but not treatment by cold storage, inhibited the potassium-induced relaxation. These results suggest that the potassium-induced relaxation of taenia caeci was due to electrogenic sodium pumping and was independent of the adrenergic innervation of the tissue.
在豚鼠离体盲肠绦虫中，过量钾离子（10 - 30 mM）会引发阶段性松弛，随后是收缩。这种阶段性松弛不受六甲铵、酚妥拉明、普萘洛尔和溴苄铵处理的影响。然而，血管周围神经刺激所诱导的松弛会被所有这些药物抑制，但六甲铵除外。河豚毒素抑制这两种形式的松弛。钾离子诱导的松弛不伴有[3H]去甲肾上腺素释放。血管周围神经刺激导致[3H]去甲肾上腺素释放，而这被溴苄铵阻断。哇巴因处理或用LiCl替代NaCl，但冷藏处理则不会，抑制了钾离子诱导的松弛。这些结果表明，钾离子诱导的盲肠绦虫松弛是由于生电性钠泵作用，且与该组织的肾上腺素能神经支配无关。
