Resveratrol Inhibits Nicotinic Stimulation-Evoked Catecholamine Release from the Adrenal Medulla.
10.4196/kjpp.2008.12.4.155
- Author:
Seong Chang WOO
1
;
Gwang Moon NA
;
Dong Yoon LIM
Author Information
1. Department of Anesthesiology and Pain Medicine, College of Medicine, Eulji University Hospital, Daejeon, Korea.
- Publication Type:Original Article
- Keywords:
Resveratrol;
Catecholamine secretion;
Adrenal medulla;
Cholinergic receptors;
Nitric oxide
- MeSH:
(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethylammonium Chloride;
3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester;
Adrenal Glands;
Adrenal Medulla;
Animals;
Calcium;
Catecholamines;
Cytoplasm;
Dihydropyridines;
Dimethylphenylpiperazinium Iodide;
Indoles;
Ions;
Neurons;
NG-Nitroarginine Methyl Ester;
Nitric Oxide;
Nitric Oxide Synthase;
Perfusion;
Rats;
Receptor, Muscarinic M1;
Receptors, Cholinergic;
Receptors, Nicotinic;
Stilbenes;
Veins;
Veratridine
- From:The Korean Journal of Physiology and Pharmacology
2008;12(4):155-164
- CountryRepublic of Korea
- Language:English
-
Abstract:
Resveratrol has been known to possess various potent cardiovascular effects in animal, but there is little information on its functional effect on the secretion of catecholamines (CA) from the perfused model of the adrenal medulla. Therefore, the aim of the present study was to determine the effect of resveratrol on the CA secretion from the isolated perfused model of the normotensive rat adrenal gland, and to elucidate its mechanism of action. Resveratrol (10~100micrometer) during perfusion into an adrenal vein for 90 min inhibited the CA secretory responses evoked by ACh (5.32 mM), high K+ (a direct membrane-depolarizer, 56 mM), DMPP (a selective neuronal nicotinic Nn receptor agonist, 100micrometer) and McN-A-343 (a selective muscarinic M1 receptor agonist, 100micrometer) in both a time- and dose- dependent fashion. Also, in the presence of resveratrol (30micrometer), the secretory responses of CA evoked by veratridine 8644 (an activator of voltage-dependent Na+ channels, 100micrometer), Bay-K-8644 (a L-type dihydropyridine Ca2+ channel activator, 10micrometer), and cyclopiazonic acid (a cytoplasmic Ca2+ -ATPase inhibitor, 10micrometer) were significantly reduced. In the simultaneous presence of resveratrol (30micrometer) and L-NAME (an inhibitor of NO synthase, 30micrometer), the CA secretory evoked by ACh, high K+, DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid were recovered to a considerable extent of the corresponding control secretion compared with the inhibitory effect of resveratrol alone. Interestingly, the amount of nitric oxide (NO) released from the adrenal medulla was greatly increased in comparison to its basal release. Taken together, these experimental results demonstrate that resveratrol can inhibit the CA secretory responses evoked by stimulation of cholinergic nicotinic receptors, as well as by direct membrane-depolarization in the isolated perfused model of the rat adrenal gland. It seems that this inhibitory effect of resveratrol is exerted by inhibiting an influx of both ions through Na+ and Ca2+ channels into the adrenomedullary cells as well as by blocking the release of Ca2+ from the cytoplasmic calcium store, which are mediated at least partly by the increased NO production due to the activation of NO synthase.
