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血管加压素对正常及地塞米松处理大鼠离体结肠电解质转运的影响。

Effects of vasopressin on electrolyte transport across isolated colon from normal and dexamethasone-treated rats.

作者信息

Bridges R J, Rummel W, Wollenberg P

出版信息

J Physiol. 1984 Oct;355:11-23. doi: 10.1113/jphysiol.1984.sp015402.

Abstract

Vasopressin enhanced the absorption of Na+ and Cl- across the short-circuited colon descendens from normal rats. This effect of vasopressin results from an increase in the mucosal to serosal movement of Na+ and Cl- and a decrease in the serosal to mucosal movement of Cl- and was accompanied with a decrease in the short-circuit current (ISC). Neither the base-line absorption of Na+ and Cl-, the vasopressin-induced increase in Na+ and Cl- absorption nor the decrease in ISC were inhibited by amiloride in the colon from normal rats. Colon descendens from rats treated for 3 days with dexamethasone had remarkably higher transmural potential difference (p.d.), tissue conductance (Gt) and ISC. The absorption of Na+ across the short-circuited colon descendens from dexamethasone-treated rats was increased 3-fold when compared to colon from normal rats. The absorption of Cl- in normal rats was reversed to Cl- secretion in treated rats. Amiloride rapidly and reversibly decreased the p.d., Gt and ISC in colon from dexamethasone-treated rats. The transport of Na+ was nearly completely inhibited by amiloride in treated rats. In contrast to its enhancing effects on Na+ absorption in colon from normal rats vasopressin did not enhance Na+ absorption in colon from dexamethasone-treated rats. This enhancement of Cl- absorption by vasopressin was retained in colon from treated rats. This enhancement of Cl- transport was due solely to a decrease in the serosal to mucosal movement of Cl- and was accompanied with a decrease in ISC and Gt. The results support the hypothesis that vasopressin causes inhibition of the electrogenic secretion of Cl- in colon from dexamethasone-treated rats. Furthermore, the results suggest that the increase in the mucosal to serosal movement of Na+ and Cl- and the decrease in the serosal to mucosal movement of Cl- in colon from normal rats are caused by independent effects of vasopressin.

摘要

血管加压素增强了正常大鼠短路降结肠对Na⁺和Cl⁻的吸收。血管加压素的这种作用源于Na⁺和Cl⁻从黏膜到浆膜的转运增加以及Cl⁻从浆膜到黏膜的转运减少,并伴有短路电流(ISC)降低。在正常大鼠的结肠中,阿米洛利既不抑制Na⁺和Cl⁻的基线吸收,也不抑制血管加压素诱导的Na⁺和Cl⁻吸收增加或ISC降低。用 dexamethasone 处理 3 天的大鼠的降结肠具有显著更高的跨膜电位差(p.d.)、组织电导(Gt)和ISC。与正常大鼠的结肠相比,dexamethasone 处理的大鼠短路降结肠对Na⁺的吸收增加了 3 倍。正常大鼠中Cl⁻的吸收在处理后的大鼠中转变为Cl⁻分泌。阿米洛利迅速且可逆地降低了dexamethasone 处理的大鼠结肠中的 p.d.、Gt 和ISC。在处理后的大鼠中,Na⁺的转运几乎被阿米洛利完全抑制。与它对正常大鼠结肠中Na⁺吸收的增强作用相反,血管加压素并未增强dexamethasone 处理的大鼠结肠中Na⁺的吸收。血管加压素对Cl⁻吸收的这种增强作用在处理后的大鼠结肠中得以保留。这种Cl⁻转运的增强仅归因于Cl⁻从浆膜到黏膜的转运减少,并伴有ISC和Gt降低。这些结果支持了血管加压素导致dexamethasone 处理的大鼠结肠中Cl⁻的电分泌受到抑制这一假说。此外,结果表明正常大鼠结肠中Na⁺和Cl⁻从黏膜到浆膜的转运增加以及Cl⁻从浆膜到黏膜的转运减少是由血管加压素的独立作用引起的。

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