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

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.