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血管活性肠肽刺激龟膀胱中的碱排泄。

Vasoactive intestinal peptide stimulates alkali excretion in turtle urinary bladder.

作者信息

Durham J H, Matons C, Brodsky W A

出版信息

Am J Physiol. 1987 Apr;252(4 Pt 1):C428-35. doi: 10.1152/ajpcell.1987.252.4.C428.

Abstract

The turtle urinary bladder possesses an active transport mechanism for the electrogenic secretion of alkali. This process is independent of exogenous Cl and Na, induced by cyclic AMP (cAMP), and potentiated in bladders from NaHCO3-loaded (alkalotic) turtles. In the present study, it is shown that the serosal addition of vasoactive intestinal peptide (VIP) induces rapidly developing parallel increases in alkali secretion and in the short-circuiting current carried by this secretion. The VIP-induced increment in alkali secretion is greater in the presence than in the absence of an exogenously added phosphodiesterase inhibitor. Additions of a cAMP analog subsequent to the VIP-induced alkali secretion fail to induce any further increase in alkalinization. These results provide evidence for the action of VIP as a hormonal up regulator of alkali excretion in the turtle urinary bladder.

摘要

龟的膀胱具有一种主动转运机制,用于碱的电分泌。该过程独立于外源性的氯和钠,由环磷酸腺苷(cAMP)诱导,并在来自加载碳酸氢钠(碱中毒)龟的膀胱中增强。在本研究中,结果表明,浆膜侧添加血管活性肠肽(VIP)可迅速导致碱分泌以及由该分泌携带的短路电流平行增加。在存在外源性添加的磷酸二酯酶抑制剂的情况下,VIP诱导的碱分泌增加幅度大于不存在该抑制剂时。在VIP诱导碱分泌之后添加cAMP类似物不能诱导碱化进一步增加。这些结果为VIP作为龟膀胱中碱排泄的激素上调调节剂的作用提供了证据。

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