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Institut für Veterinär-Physiologie, Universität Giessen, D-35392 Giessen, Germany
The effect of
epinephrine on transport of K+,
Na+,
Cl
, and
HCO3 across the rat colon was studied
using the Ussing chamber technique. Epinephrine (5 × 106 mol/l) 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 bumetanide administration, indicating a transient
induction of Cl secretion.
The second phase of the response to epinephrine was suppressed by
apical administration of the K+
channel blocker, quinine, and was concomitant with an increase in
serosal-to-mucosal Rb+ flux,
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 mucosal-to-serosal and
serosal-to-mucosal Cl
fluxes when treated with epinephrine. In the distal colon, indomethacin abolished the first phase of the epinephrine effect, whereas the second
phase was suppressed by TTX. In the proximal colon, indomethacin and
TTX were ineffective. The neuronally mediated response to epinephrine
in the distal colon was suppressed by the nonselective 
-receptor
blocker, propranolol, and by the
2-selective blocker, ICI-118551, whereas the epithelial response in the proximal colon was
suppressed by the nonselective 
-blocker, phentolamine, and by the
selective 2-blocker, yohimbine.
These results indicate a segment-specific action of epinephrine on ion
transport: a direct stimulatory action on epithelial
2-receptors in the proximal colon and an indirect action on secretomotoneurons via
2-receptors in the distal colon.
enteric nervous system; chloride transport; potassium transport; prostaglandins
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