Nervous control of alkaline secretion in the duodenum as studied by the use of cholera toxin in the anaesthetized rat

Abstract

There is experimental evidence for an axon reflex control of alkaline secretion in the rat duodenum. We have investigated if there is also an intramural reflex control of alkaline secretion similar to that demonstrated with regard to the control of the fluid transport in the rat jejunum. Alkaline secretion in the duodenum of an anesthetized rat was continuously monitored using an in situ titration technique. The segment was extrinsically denervated. Exposing the duodenal segment to 80 microg cholera toxin markedly increased alkaline secretion. This response was abolished by hexamethonium (28 micromol (10 mg) kg(-1) body wt), a nicotinic receptor blocker, lidocaine (0.5 mL of a 1% solution on the serosal surface), a local anaesthetic, and nifedipine (5.75 micromol (2 mg) kg(-1) body wt i.v.), a calcium channel blocker. The response to cholera toxin was partially abolished by granisetron (0.11 micromol (40 microg) kg(-1) body wt i.v.), a 5-HT3 receptor blocker. Atropine (1.7 micromol (0.5 mg) kg(-1) body wt i.v.), a muscarinic receptor blocker, had no effect. We therefore conclude that the alkaline secretion in the rat jejunum evoked by cholera toxin exhibits the same pharmacological properties as the fluid secretion caused by the toxin in the jejunum. This suggests that the alkaline secretion in the rat duodenum is controlled not only by an axon reflex but also by an intramural secretory reflex similar to that controlling fluid transport in the rat jejunum.

COX inhibition excites enteric nerves that affect motility, alkaline secretion, and permeability in rat duodenum

“…Higher luminal concentrations of lidocaine did, however, reduce basal DMAS. These results confirm previous findings in the rat (9,14) and suggest that DMAS may be influenced by neural mechanisms. Interestingly, in indomethacintreated animals, a reduction of DMAS was obtained already at a luminal lidocaine concentration of 0.03% and 0.1% lidocaine almost abolished indomethacinstimulated DMAS.…”

Involvement of serotonin and calcium channels in the intestinal fluid secretion evoked by bile salt and cholera toxin

“…in a dose of 0.11 μmol (40 μg) per kg. The use of this dose was based on dose‐response curve for granisetron determined with regard to its inhibitory effect on the duodenal bicarbonate secretion ( Jaup et al ., 1998 ) and on the intestinal fluid secretion caused by cholera toxin ( Sjöqvist et al ., 1992 ). Furthermore, in the latter study the dose used attenuated the bradycardia evoked by i.v.…”

Enteric Nerves and Diarrhoea

“…Jaup et al (1998) investigated the effect of cholera toxin on bicarbonate (alkaline) transport in the duodenum. Cholera toxin evoked an increased bicarbonate secretion.…”

“…Accordingly, a low luminal pH in the duodenum evokes a nervously mediated secretion of bicarbonate ions, probably via an axon reflex (Takeuchi et al 1991;Fändriks et al 1994). Jaup et al (1998) investigated the effect of cholera toxin on bicarbonate (alkaline) transport in the duodenum. Cholera toxin evoked an increased bicarbonate secretion.…”