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Four response stages of capsaicin‐sensitive primary afferent neurons to capsaicin and its analog: Gastric acid secretion, gastric mucosal damage and protection
Author(s) -
Mózsik Gyula,
Vincze Áron,
Szolcsányi János
Publication year - 2001
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1046/j.1440-1746.2001.02598.x
Subject(s) - capsaicin , gastric acid , medicine , stimulation , pharmacology , pylorus , sensory neuron , gastric mucosa , stomach , endocrinology , receptor
Capsaicin is the active component of red hot peppers, which modifies specifically the capsaicin‐sensitive sensory afferent nerves. The action of capsaicin is an initial short‐lasting stimulation, which is followed by desensitization to capsaicin itself, and to other stimuli of afferent sensory nerves. Four response stages of capsaicin‐sensitive primary afferents exist to capsaicin, depending on the dose and duration of exposure to the drug. These are excitation, a sensory blocking effect, long‐term selective neurotoxic impairment, and irreversible cell destruction. The possible roles of four stages of capsaicin‐sensitive primary afferents can be evaluated in relation to gastric acid secretion, and to the details of the defensive side of gastric mucosa against different chemicals, physical agents, drugs and other pathological stress. Capsaicin inhibited the gastric acid secretion in pylorus‐ligated rats when it was given intragastrically at a dose of 0.4–1.8 μg/kg. Small doses of capsaicin (up to 800 μg, i.g.) produced a dose‐dependent inhibition (ID 50 = 400 μg), and its inhibitory effect was exerted for 1 h in healthy human subjects. While a small dose (5 μg/kg) of capsaicin caused inhibition, a high dose (50–100 mg/kg) enhanced the gastric mucosal lesions productivity by causing hyperacidity in pylorus‐ligated animals. Capsaicin and its analog inhibited the development of different chemically induced gastric mucosal damage in various experimental models if they were given intragastric doses (μg/kg). The final effects of capsaicin depend on the dosage and timing. The different effects are excitation, a sensory‐blocking effect, long‐term selective neurotoxic impairment and irreversible cell destruction.