The effects of capsaicin on sensory neurons are mediated by its interaction with a specific membrane receptor and opening of nonselective cation channel. In the rat heart, capsaicin-sensitive nerve endings are known to be activated by oxygen radicals. We investigated the possibility that free oxygen radicals stimulate sensory nerve endings by acting upon the capsaicin receptor. We studied the effects of capsaicin (0.1-10 μg), bradykinin (1-10 μg), H2O2 (3mmol), and xanthine + xanthine oxidase (X+XO, 20 mmol + 0.03 mU) applied to the surface of the heart for 30 sec on the activity of cardiac capsaicin-sensitive vagal and sympathetic afferent fibers before and after blockade of capsaicin receptors with capsazepine (2 mg/kg, iv). Application of capsaicin (10 ug) increased vagal fibers activity by 427%, H2O2 by 87%, X+XO by 466%, and bradykinin (10 μg) by 127%. Administration of capsapine had no affect on the baseline activity of the tested fibers, but it completely abolished the responses of vagal afferent fibers to capsaicin, H,O, and X+XO. Capsazepine had no effect on the responses to bradykinin". The response of sympathetic afferent fibers to capsaicin and H,O, also was abolished by capsazepine, while their response to bradykinin was not affected. The results of these experiments indicate that blockade of capsaicin receptors inhibits activation of vagal and sympathetic cardiac afferent Fibers by free oxygen radicals. The fact that capsazepine did not affect the afferent response to bradykinin suggests that this effect of the blocker was specific for capsaicin receptors.
|Original language||English (US)|
|State||Published - 1996|
ASJC Scopus subject areas
- Molecular Biology