Effects of histamine and histamine receptor antagonists on ion transport in rabbit descending colon.

Effects of histamine and histamine receptor antagonists on ion transport in rabbit descending colon.
复制标题

组胺和组胺受体拮抗剂对兔降结肠离子转运的影响。

DOI:
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发表时间:
1984
影响因子:
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通讯作者:
P. Smith
P. Smith
中科院分区:
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文献类型:
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作者:
R. McCabe;P. Smith

文献摘要

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在离体兔降结肠标本上观察了组胺对结肠离子转运的影响。血清中加入组胺(10(-5)M)可引起短路电流(Isc)和跨上皮电导的短暂增加。通过从两种浴液中去除Cl,在Serbine浴液中加入呋塞米(10(-3)M),在Serbine和粘膜浴液中加入吲哚美辛(10(-5)M),或从Serbine浴液中去除Ca,可以阻断Isc对组胺的反应。此外,H1受体拮抗剂苯海拉明以剂量依赖性方式抑制组胺诱导的Isc增加,最大抑制浓度为10(-4)M,半最大抑制浓度为3 × 10(-7)M。H2受体拮抗剂西咪替丁(10(-3)M)对组胺反应无影响。单向Na、K和Cl通量的测量显示,由于粘膜-丝氨酸Na通量的减少,丝氨酸加入苯海拉明(10(-3)M)降低了基础Isc。浆液中加入苯海拉明(10(-3)M)也可抑制浆液中加入前列腺素E1、8-溴-cAMP、霍乱毒素或离子载体A23187产生的Isc增加。单向K和Cl通量的测量显示,前列腺素E1单独增加浆膜-粘膜K和Cl通量,减少粘膜-浆膜K通量,从而增加净K和Cl分泌。苯海拉明(10(-3)M)消除了前列腺素E1产生的Cl通量的变化,并降低了K通量变化的幅度。(250字处删节)
The effects of histamine on colonic ion transport were examined in in vitro preparations of rabbit descending colon. Serosal addition of histamine (10(-5) M) produced a transient increase in short-circuit current (Isc) and transepithelial conductance. The Isc response to histamine could be blocked by removing Cl from both bathing solutions, adding furosemide (10(-3) M) to the serosal bathing solution, adding indomethacin to the serosal and mucosal bathing solutions (10(-5) M), or removing Ca from the serosal bathing solution. In addition, the histamine-induced increase in Isc was inhibited in a dose-dependent manner by the H1-receptor antagonist diphenhydramine, with a maximal inhibition at 10(-4) M and a half-maximal inhibition at 3 X 10(-7) M. The H2-receptor antagonist cimetidine (10(-3) M) was without effect on the histamine response. Measurement of unidirectional Na, K, and Cl fluxes revealed that serosal addition of diphenhydramine (10(-3) M) reduced basal Isc due to a decrease in mucosal-to-serosal Na flux. Serosal addition of diphenhydramine (10(-3) M) also inhibited the increase in Isc produced by serosal addition of prostaglandin E1, 8-bromo-cAMP, cholera toxin, or the ionophore A23187. Measurement of unidirectional K and Cl fluxes revealed that prostaglandin E1 alone increased serosal-to-mucosal K and Cl fluxes and reduced the mucosal-to-serosal K flux, thereby increasing net K and Cl secretion. Serosal diphenhydramine (10(-3) M) abolished the changes in Cl fluxes produced by prostaglandin E1 and reduced the magnitude of the changes in K fluxes.(ABSTRACT TRUNCATED AT 250 WORDS)