Capsaicin inhibits catecholamine secretion and synthesis by blocking Na+ and Ca2+ influx through a vanilloid receptor-independent pathway in bovine adrenal medullary cells

@article{Takahashi2006CapsaicinIC,
  title={Capsaicin inhibits catecholamine secretion and synthesis by blocking Na+ and Ca2+ influx through a vanilloid receptor-independent pathway in bovine adrenal medullary cells},
  author={Kojiro Takahashi and Yumiko Toyohira and Susumu Ueno and Masato Tsutsui and Nobuyuki Yanagihara},
  journal={Naunyn-Schmiedeberg's Archives of Pharmacology},
  year={2006},
  volume={374},
  pages={107-116}
}
We report here the effects of capsaicin, a flavoring ingredient in the hot pepper Capsicum family, on catecholamine secretion and synthesis in cultured bovine adrenal medullary cells. Capsaicin inhibited catecholamine secretion (IC50=9.5, 11.8, and 62 μM) stimulated by carbachol, an agonist of the nicotinic acetylcholine receptor, by veratridine, an activator of voltage-dependent Na+ channels, and by high K+, an activator of voltage-dependent Ca2+ channels, respectively. Capsaicin also… 

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References

SHOWING 1-10 OF 36 REFERENCES

Capsaicin inhibits phospholipase C-mediated Ca(2+) increase by blocking thapsigargin-sensitive store-operated Ca(2+) entry in PC12 cells.

  • S. ChoiK. T. Kim
  • Biology, Chemistry
    The Journal of pharmacology and experimental therapeutics
  • 1999
The results suggest that capsaicin does not mediate vanilloid receptor signaling when inhibiting the thapsigargin-sensitive SOCE subsequent to phospholipase C activation.

Selective blockade of nicotinic acetylcholine receptors by pimobendan, a drug for the treatment of heart failure: reduction of catecholamine secretion and synthesis in adrenal medullary cells

It is suggested that pimobendan inhibits carbachol-induced catecholamines secretion and synthesis through suppression of nicotinic acetylcholine receptors.

Capsaicin-, Resiniferatoxin-, and Olvanil-induced Adrenaline Secretions in Rats via the Vanilloid Receptor

The results suggest that some vanilloids (capsaicin, resiniferatoxin, olvanil) excite adrenaline secretion and such excitation is via the vanilloid receptor.

Inhibitory effects of tramadol on nicotinic acetylcholine receptors in adrenal chromaffin cells and in Xenopus oocytes expressing α7 receptors

Tramadol inhibits catecholamine secretion partly by inhibiting nicotinic AChR functions in a naloxone‐insensitive manner and α7 receptors are one of those inhibited by tramadol.

A Neurosteroid Anesthetic, Alphaxalone, Inhibits Nicotinic Acetylcholine Receptors in Cultured Bovine Adrenal Chromaffin Cells

It is concluded that alphaxalone, at anesthetic concentrations, inhibits nAChRs in adrenal chromaffin cells, and may affect the sympathetic and other nervous systems via inhibition of nA ChRs.

Effects of capsaicin on Ca(2+) release from the intracellular Ca(2+) stores in the dorsal root ganglion cells of adult rats.

Caffeine completely abolished capsaicin-induced [Ca(2+)](i) transient and depletion of IP(3)-sensitive Ca(2+) stores by bradykinin and phospholipase C inhibitors, neomycin, and U-73122, did not block capsicin- induced [Ca (2+) transient, in conclusion.

Adrenal sympathetic efferent nerve and catecholamine secretion excitation caused by capsaicin in rats.

The results suggest that the enhancement of physiological catecholamine secretion by capsaicin is mainly through activation of the central nervous system.

Spatial localization of agonist-induced Ca2+ entry in bovine adrenal chromaffin cells. Different patterns induced by histamine and angiotensin II, and relationship to catecholamine release.

The results directly demonstrate that different agonists can induce different patterns of divalent cation influx in the same cells and, furthermore, suggest how these different patterns can have a direct influence on cellular function.