Vianna-Jorge R, Oliveira C F, Garcia M L, Kaczorowski G J, Suarez-Kurtz G
Coordenação de Pesquisa, Instituto Nacional de Câncer, Rio de Janeiro, Praça da Cruz Vermelha 23, Rio de Janeiro, RJ 20230-130, Brazil.
Br J Pharmacol. 2000 Oct;131(4):772-8. doi: 10.1038/sj.bjp.0703620.
Correolide (1 - 10 microM), a nortriterpene purified from Spachea correae and a selective blocker of Kv1 potassium channels, elicits repetitive twitching in guinea-pig ileum. This effect is not seen in guinea-pig duodenum, portal vein, urinary bladder or uterine strips, nor in rat or mouse ileum. The time course and amplitude of the correolide-induced twitches in guinea-pig ileum are similar to those elicited by electrical stimulation of the enteric nervous system. The correolide-induced twitching is not affected by pre-treatment with capsaicin (1 microM), but is facilitated by the NO synthase inhibitor, N(G)-nitro-L-arginine methyl esther (L-NAME, 200 microM). The correolide-induced twitching is abolished by tetrodotoxin (1 microM) or hexamethonium (100 microM), and is markedly inhibited by nifedipine (0.3 microM) or atropine (0.2 microM). The atropine-resistant component is inhibited by selective antagonists of NK1 and NK2 tachykinin receptors, namely GR 82334 and GR 94800 (1 microM each). The former compound is more effective in inhibiting the correolide-induced, atropine-resistant activity. Correolide intensified the twitching of ileum segments exposed to saturating concentrations of margatoxin (MgTX), which suggests that Kv1 sub-types other than Kv1.1 (Kv1.4 or Kv1.5) are involved in the relatively greater degree of stimulation of the enteric nervous system by correolide, as compared to MgTX. We propose that blockade of Kv1 channels by correolide increases the excitability of intramural nerve plexuses promoting release of acetylcholine and tachykinins from excitatory motor neurons. This, in turn, leads to Ca(2+)-dependent action potentials and twitching of the muscle fibres.
从 Spachea correae 中纯化得到的降三萜类化合物 correolide(1 - 10 microM)是一种 Kv1 钾通道的选择性阻滞剂,可引起豚鼠回肠反复抽搐。在豚鼠十二指肠、门静脉、膀胱或子宫条带以及大鼠或小鼠回肠中未观察到这种效应。correolide 诱导的豚鼠回肠抽搐的时间进程和幅度与肠神经系统电刺激引起的相似。correolide 诱导的抽搐不受辣椒素(1 microM)预处理的影响,但一氧化氮合酶抑制剂 N(G)-硝基-L-精氨酸甲酯(L-NAME,200 microM)可促进其发生。correolide 诱导的抽搐可被河豚毒素(1 microM)或六甲铵(100 microM)消除,并被硝苯地平(0.3 microM)或阿托品(0.2 microM)显著抑制其中对阿托品耐药的成分可被 NK1 和 NK2 速激肽受体的选择性拮抗剂 GR 82334 和 GR 94800(各 1 microM)抑制。前一种化合物在抑制 correolide 诱导的、对阿托品耐药的活性方面更有效。Correolide 增强了暴露于饱和浓度玛格毒素(MgTX)的回肠段的抽搐,这表明与 MgTX 相比,除 Kv1.1 之外的 Kv1 亚型(Kv1.4 或 Kv1.5)在 correolide 对肠神经系统的相对更大程度刺激中起作用。我们认为,correolide 对 Kv1 通道的阻断增加了壁内神经丛的兴奋性,促进乙酰胆碱和速激肽从兴奋性运动神经元释放。这反过来又导致依赖钙的动作电位和肌肉纤维的抽搐。