Cholinergic-adrenergic interactions on intestinal ion transport

The autonomic control of intestinal electrolyte transport has been investigated in the in vitro, short-circuited rabbit ileum with varying doses of carbachol and with neuroeffector blocking agents. Low-dose carbachol (<10^-6 M) and high-dose carbachol (>10^-4 M) had different effects on Na and Cl transport. Low-dose carbachol caused a transient increase in the potential difference and short-circuit current, stimulated Cl secretion, and inhibited the residual flux (probably HCO₃ secretion). This is a muscarinic response since it is inhibited by atropine (10^-6 M). After an initial increase of the potential difference and short-circuit current, high-dose carbachol reduced these electrical parameters, stimulated Na and Cl absorption, and abolished the residual flux. This is a nicotinic response since it is inhibited by hexamethonium (10^-5 M). This nicotinic response is identical to that reported by others with α-adrenergic agents and it was inhibited also by phentolamine (10^-7 M). The authors propose high-dose carbachol stimulates nicotinic receptors on postganglionic sympathetic fibers present in their preparations causing a release of catecholamines and a resulting α-adrenergic response by the intestinal epithelial cell. The physiological significance of this response in the gut remains to be determined.