霍乱的抑制toxin-induced 5 -释放的5 -(3)受体拮抗剂,granisetron,老鼠。

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Turvill JL康纳P一分钱乔丹

霍乱的抑制toxin-induced 5 -释放的5 -(3)受体拮抗剂,granisetron,老鼠。

Br J杂志。2000年7月,130 (5):1031 - 6。

PubMed ID

10882387 (在PubMed

]

文摘

1。的促分泌素5 -羟色胺(5 -)是涉及的病理生理学霍乱。霍乱毒素暴露后5 -释放肠嗜铬细胞的细胞被认为激活non-neuronally(5 -(2)依赖)和神经元(5 -(3)依赖)介导的水和电解质的分泌。可以减少CT-secretion防止释放5 -。肠嗜铬细胞的细胞具有许多受体,在基础条件下,调节5 -释放。2。这些基底包括5 -(3)受体,激活的增强5 -释放。3所示。直到现在,5 -(3)受体拮抗剂(如granisetron)认为霍乱toxin-induced液体分泌抑制了封锁5 -(3)分泌肠神经元受体。相反,我们认为他们的行为通过抑制霍乱toxin-induced肠嗜铬细胞的细胞脱粒。 4. Isolated intestinal segments in anaesthetized male Wistar rats, pre-treated with granisetron 75 microg kg(-1), lidoocaine 6 mg kg(-1) or saline, were instilled with a supramaximal dose of cholera toxin or saline. Net fluid movement was determined by small intestinal perfusion or gravimetry and small intestinal and luminal fluid 5-HT levels were determined by HPLC with fluorimetric detection. 5. Intraluminal 5-HT release was proportional to the reduction in tissue 5-HT levels and to the onset of water and electrolyte secretion, suggesting that luminal 5-HT levels reflect enterochromaffin cell activity. 6. Both lidocaine and granisetron inhibited fluid secretion. However, granisetron alone, and proportionately, reduced 5-HT release. 7. The simultaneous inhibition of 5-HT release and fluid secretion by granisetron suggests that 5-HT release from enterochromaffin cells is potentiated by endogenous 5-HT(3) receptors. The accentuated 5-HT release promotes cholera toxin-induced fluid secretion.

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药物靶点

药物	目标	类	生物	药理作用	行动
Granisetron	5 -羟色胺受体3	蛋白质	人类	是的	拮抗剂	细节