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Influence of capsaicin‐sensitive afferent neurones on the acid secretory responses of the rat stomach in vivo
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The influence of capsaicin‐sensitive afferent neurones in modulating acid‐secretory responses has been investigated in the continuously perfused stomach of the anaesthetized rat.
Ablation of primary afferent neurones, after systemic neonatal pretreatment with high doses of capsaicin, did not modify acid responses to direct stimuli of the oxyntic cell with histamine (5 mg kg_1), pentagastrin (20 μg kg−1) or carbachol (4 μg kg−1).
Acid responses to hypoglycaemia induced by insulin (0.3 iu kg−1) were not influenced by systemic capsaicin pretreatment or by acute coeliac ganglionectomy. Vagotomy abolished this secretory response.
The increase in acid output induced by gastric distension (20 cmH2O) was abolished by systemic neonatal capsaicin pretreatment. Likewise, vagotomy and acute coeliac ganglionectomy eliminated this secretory response.
Acute intragastric infusion with high doses of capsaicin inhibited the acid responses to distension but failed to modify the increase in acid output induced by insulin.
Local application (7–14 days before) of capsaicin to the coeliac ganglion abolished the acid response to gastric distension. This lack of secretory response was not the result of a nonspecific destruction of the ganglion, since changes in intragastric pressure after electrical stimulation of the coeliac ganglion were unaffected by such treatment.
These observations indicate that peripheral capsaicin‐sensitive sensory neurones, located both in the gastric mucosa and in the coeliac ganglion, play a physiological role in the acid secretory responses to gastric distension.
Title: Influence of capsaicin‐sensitive afferent neurones on the acid secretory responses of the rat stomach in vivo
Description:
The influence of capsaicin‐sensitive afferent neurones in modulating acid‐secretory responses has been investigated in the continuously perfused stomach of the anaesthetized rat.
Ablation of primary afferent neurones, after systemic neonatal pretreatment with high doses of capsaicin, did not modify acid responses to direct stimuli of the oxyntic cell with histamine (5 mg kg_1), pentagastrin (20 μg kg−1) or carbachol (4 μg kg−1).
Acid responses to hypoglycaemia induced by insulin (0.
3 iu kg−1) were not influenced by systemic capsaicin pretreatment or by acute coeliac ganglionectomy.
Vagotomy abolished this secretory response.
The increase in acid output induced by gastric distension (20 cmH2O) was abolished by systemic neonatal capsaicin pretreatment.
Likewise, vagotomy and acute coeliac ganglionectomy eliminated this secretory response.
Acute intragastric infusion with high doses of capsaicin inhibited the acid responses to distension but failed to modify the increase in acid output induced by insulin.
Local application (7–14 days before) of capsaicin to the coeliac ganglion abolished the acid response to gastric distension.
This lack of secretory response was not the result of a nonspecific destruction of the ganglion, since changes in intragastric pressure after electrical stimulation of the coeliac ganglion were unaffected by such treatment.
These observations indicate that peripheral capsaicin‐sensitive sensory neurones, located both in the gastric mucosa and in the coeliac ganglion, play a physiological role in the acid secretory responses to gastric distension.
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