Nat Prod Sci.  2021 Jun;27(2):86-98. 10.20307/nps.2021.27.2.86.

Suppressive Impact of Ginsenoside-Rg2 on Catecholamine Secretion from the Rat Adrenal Medulla

  • 1Department of Psychiatry, College of Medicine, Chosun University, Gwangju 61453, Korea
  • 2Division of Hematology/Medical Oncology, Department of Internal Medicine, Seoul National University Boramae Medical Center, Seoul 07061, Korea
  • 3Department of Internal Medicine (Division of Pulmonary and Critical Care Medicine), Veterans Health Service Medical Center, Seoul 05368, Korea
  • 4Department of Internal Medicine (Division of Cardiology), College of Medicine, Chosun University, Gwangju 61453, Korea
  • 5Department of Pharmacology, College of Medicine, Chosun University, Gwangju 61452, Korea


This study was designed to characterize the effect of ginsenoside-Rg2 (Rg2), one of panaxatriol saponins isolated from Korean ginseng root, on the release of catecholamines (CA) in the perfused model of the rat adrenal medulla, and also to establish its mechanism of action. Rg2 (3~30 µM), administered into an adrenal vein for 90 min, depressed acetylcholine (ACh)-induced CA secretion in a dose- and time-dependent manner. Rg2 also time-dependently inhibited the CA secretion induced by 3-(m-chloro-phenyl-carbamoyl-oxy)-2-butynyltrimethyl ammonium chloride (McN-A-343), 1.1-dimethyl-4-phenyl piperazinium iodide (DMPP), and angiotensin II (Ang II). Also, during perfusion of Rg2, the CA secretion induced by high K+ , veratridine, cyclopiazonic acid, methyl-1,4-dihydro-2,6-dimethyl-3-nitro-4-(2-trifluoro-methyl-phenyl)-pyridine-5-carboxylate (Bay-K-8644) depressed, respectively. In the simultaneous presence of Rg2 and Nω -nitro-L-arginine methyl ester hydrochloride (L-NAME), the CA secretion induced by ACh, Ang II, Bay-K-8644 and veratridine was restored nearly to the extent of their corresponding control level, respectively, compared to those of inhibitory effects of Rg2-treatment alone. Virtually, NO release in adrenal medulla following perfusion of Rg2 was significantly enhanced in comparison to the corresponding spontaneous release. Also, in the coexistence of Rg2 and fimasartan, ACh-induced CA secretion was markedly diminished compared to the inhibitory effect of fimasartantreated alone. Collectively, these results demonstrated that Rg2 suppressed the CA secretion induced by activation of cholinergic as well as angiotensinergic receptors from the perfused model of the rat adrenal gland. This Rg2-induced inhibitory effect seems to be exerted by reducing both influx of Na + and Ca 2+ through their ionic channels into the adrenomedullary cells as well as by suppressing Ca 2+ release from the cytoplasmic calcium store, at least through the elevated NO release by activation of NO synthase, which is associated to the blockade of neuronal cholinergic and AT 1 -receptors. Based on these results, the ingestion of Rg2 may be helpful to alleviate or prevent the cardiovascular diseases, via reduction of CA release in adrenal medulla and consequent decreased CA level in circulation.


Ginsenoside-Rg2; adrenal medulla; catecholamine secretion; NO release
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