Die segmentspezifischen Wirkungen von Adrenalin auf den Ionentransport am Colon der Ratte

Abstract

The effect of epinephrine on transport of K⁺, Na⁺, Cl^- and HCO3^- across the colon of the rat was studied with the Ussing chamber technique. Epinephrine (5.10^-6 mol.l^-1) induced a biphasic change in short-circuit current (Isc) in distal and proximal colon: a transient increase followed by a long-lasting decay. The first phase of the Isc response was abolished in Cl^--poor solution or after administration of bumetanide, an inhibitor of the Na⁺-K⁺-2 Cl^- cotransporter, indicating a transient induction of Cl^- secretion. The 2. phase of the response to epinephrine was suppressed by administration of the K⁺ channel blocker, quinine, and was concomitant with an increase in J^Rb_sm indicating that epinephrine induced K⁺ secretion, although this response was much smaller than the change in Isc. In addition, the distal colon displayed a decrease in J^Cl_ms and J^Cl_sm when treated with epinephrine.

In the distal colon indomethacin, a cyclooxygenase inhibitor, abolished the 1. phase of the epinephrine effect, whereas the 2. phase was suppressed by tetrodotoxin. In the proximal colon indomethacin and tetrodotoxin were in-effective. The neuronally-mediated response to epinephrine in the distal colon was suppressed by the non-selective [beta]-receptor blocker, propranolol, and by the [beta]₂-selective blocker, ICI 118551, whereas the epithelial response in the proximal colon was suppressed by the non-selective [alpha]-blocker, phentolamine, and by the selective [alpha]₂-blocker, yohimbine.

These results indicate a segment-specific action of epinephrine on ion transport: an indirect action on secretomotor neurons via [beta]₂-receptors in the distal and a direct stimulatory action on epithelial [alpha]₂-receptors in the proximal colon.

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