Gastric acid secretory responses induced by peptone are mediated by capsaicin-sensitive sensory afferent neurons

Abstract

The involvement of capsaicin-sensitive afferent neurons in modulating acid-secretory responses to peptone, a product of protein digestion, has been investigated in the continuously perfused stomach of the urethan-anesthetized rat. Systemic neonatal pretreatment with capsaicin, which destroys primary afferent neurons, does not modify basal levels of acid secretion. Acid responses to intragastric perfusion with isotonic (0.5, 1, and 2.4%) or hypertonic (10 and 20%) solutions of peptone were reduced in capsaicin-treated rats. Intragastric perfusion with hypertonic mannitol (18%) did not stimulate secretion of acid. Systemic capsaicin pretreatment did not modify acid responses to intraperitoneal histamine (5 mg/kg) or pentagastrin (100 micrograms/kg). Acute intragastric perfusion (10 min) with capsaicin (0.3 mg/ml), tetrodotoxin (150 ng/ml), or the combination of both neurotoxins reduced the acid responses to 1% peptone to levels not different from those of animals treated systemically with capsaicin. Bilateral vagotomy or acute celiac ganglionectomy also decreased acid responses to 1% peptone in control animals, without modifying the diminished responses to peptone in rats treated systemically with capsaicin. Gastric acid secretory responses in rats undergoing both vagotomy and celiac ganglionectomy were not lower than those obtained after each surgical procedure alone. These findings suggest that peptone stimulates acid secretion in the rat partially by activating a nervous reflex mediated by capsaicin-sensitive sensory afferent fibers. The reflex arc involves fibers that would terminate in the gastric mucosa and project to, or from, the central nervous system through the vagus and the celiac ganglion.

Acid-Sensing Properties in Rat Gastric Sensory Neurons from Normal and Ulcerated Stomach

“…In contrast with the results of Benson et al (1999), who noted acid-elicited currents in 74% of cardiac NG neurons, all gastric NG neurons studied here responded to acid. Interestingly, gastric NG neurons generated action potentials in response to depolarizing current injections or additional increases in proton concentration even after prolonged exposure to pH 6.6, which may reflect the importance of gastric vagal afferents in the regulation of acid secretion and in chemonociception (Ramos et al, 1992;Holzer, 2002;Schicho et al, 2004).…”

Capsaicin and Gastric Ulcers

“…nerves have no influence on the basal or stimulated acid secretion by histamine and pentagastrin. 239 Perfusion, g.i. or serosal application of capsaicin has no effect on the acid secretion caused by electrical stimulation of the vagus nerve.…”

“…nerves has no effect on acid secretion induced by 2-deoxy-D-glucose, 73 histamine in small doses of 0.1 mg/Kg or 5 mg/Kg at which it directly activates oxyntic cells, 236,239 carbachol, 40,193,236 pentagastrn, 236,239 pentapstrin, 76 secretory response due to hypoglycemia induced by insulin, 40 acid and pepsin secretion by bethenecol, 237 in the damaged stomach 115 and by electrical vagal stimulation. 184,237 …”

“…130 Bilateral vagotomy and acute celiac ganglionectomy decrease acid response to 1% peptone in control rats without affecting in capsaicin pre treated rat. 239 …”

Tachykinins in regulation of gastric motility and secretion

“…Sensory afferent nerve fibers therefore seem to be involved in reflex regulation of acid secretion induced by distension. Also, inhibition of acid secretion by acidification of the small intestine and stimulated acid secretion by protein (peptone) in the stomach seem to be influenced by sensory nerve fibers [86,87]. These effects may be mediated by vagal sensory nerves stimulated antidromically, because acid secretion induced by electrical stimulation of the vagus nerves could be inhibited by pretreatment of the vagus nerves with capsaicin.…”