• Archives of Pharmacal Research
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• v.12 no.3
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• pp.166-175
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• 1989

In the previous observations, it was reported that both total ginseng saponin and panaxadiol revealed the marked secretory effect of catecholamines (CA) from the rabbit adrenal gland and that CA secretion induced by them is due to dual mechanisms, cholinergic action and the direct action. In the present study, an attempt to investigate the effect of panaxatriol-type saponin (PT), which is known as an active component of Korean ginseng, on the secretion of CA from the rabbit adrenal gland was made. PT(200 $\mu$g) administered into adrenal vein evoked significantly secretion of CA from the isolated perfused rabbit adrenal gland. Secretory effect of CA produced by PT was attenuated clearly by treatment with chlorisondamine or adenosine, but was markedly increased by physostigmine. Perfusion of Krebs solution containing PT (200 $\mu$g) for 30 min potentiated greatly secretion of CA induced by acetylcholine. PT-induced CA secretion was weakened considerably by ouabain treatement or perfusion of calcium-free Krebs solution. These experimental data demonstrate that PT releases CA from the isolated perfused rabbit adrenal gland by a calcium-dependentd exocytotic mechanism. It seems that the secretory effect of PT is caused through the release of acetylcholine form cholinergic terminals present in the adrenal gland and a direct action on the chromaffin cell itself.

• Proceedings of the Ginseng society Conference
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• 2002.10a
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• pp.401-415
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• 2002

Lim and his coworkers (1987; 1988; 1989) have also found that all of total Ginseng saponin, panaxadiol-and panaxatriol-type saponins cause the increased secretion of catecholamines (CA) in a $Ca^{2+}$ -dependent fashion from the isolated perfused rabbit adrenal glands through the activation of cholinergic (both nicotinic and muscarinic) receptors. These CA secretory effects are partly due to the direct action on the rabbit adrenomedullary chromaffin cells. However, the present study was designed to examine the effect of total ginseng saponin on CA secretion evoked by activation of cholinergic nicotinic receptors in the isolated perfused model of the rat adrenal gland. Total ginseng saponin given (100 ${\mu}g$/20 min) into an adrenal vein did fail to produce alteration of spontaneous CA release from the rat adrenal medulla. Acetylcholine(5.32 mM)- and DMPP(100 ${\mu}M$, a selective nicotinic receptor agonist)-evoked CA secretory responses were reduced markedly after the pretreatment with the total ginseng saponin at a rate of 100 ${\mu}g$/6.2 ml/20 min, respectively. Pretreatment with total ginseng saponin also depressed greatly high potassium (56 mM, a membrane depolarizing agent)- and Bay-K-8644 (10 ${\mu}M$, a calcium channel activator)-induced CA secretions. Taken together, it is thought that total ginseng saponin can inhibit the releasing effect of CA evoked by nicotinic receptor stimulation from the isolated perfused rat adrenal medulla, which seems to be associated to the direct inhibition of influx through L-type calcium channel into the rat adrenomedullary chromaffin cells. It seems that there is species differences in the adrenomedullary catecholamine secretion between the rabbit and rat.

• Journal of Ginseng Research
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• v.26 no.4
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• pp.178-186
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• 2002

The present study was attempted to investigate the effects of total ginseng saponin (G75), panaxadiol-type (PDS) and panaxatriol-type saponin (PTS) on contractile responses of vasoconstrictors in aortic smooth muscle stripes of normotensive (NR) and spontaneous hypertensive rats (SHR). Phenylephrine (an adrenergic $\alpha$$\_$1/-receptor agonist) and high potassium (a membrane depolarizing agent) caused greatly contractile responses in both NR and AHR aorta, respectively. Phenylephrine- and high potassium-induced contractile responses were greater in NA than those in SHR aortic smooth muscle stripes. In NR, the contractile responses of high potassium (5.6$\times$10$\^$-2/ M) were not affected in the presence of GTS (300 $\mu$g/ml), PDS (300 $\mu$g/ml), and PTS (300 $\mu$g/ml), respectively whereas phenylephrine (10$\^$-6/ M)-induced contractile responses were markedly inhibited. In SHR, the contractile responses of high potassium (5.6$\times$10$\^$-2/ M) were not affected in the presence of GTS (300 $\mu$g/ml), PDS (300 $\mu$g/ml), and moderate doses of PTS (150-300 $\mu$g/ml), respectively but greatly blocked by high concentration of PTS (600 $\mu$g/ml). Phenylephrine (10$\^$-6/ M)-induced contractile responses were inhibited in a dose dependent fashion (150-600 $\mu$g/ml) by the pretreatment with PTS while not altered in the presence of GTS (300 $\mu$g/ml) and PDS (300 $\mu$g/ml), respectively. Taken together, these experimental results suggest that ginseng saponins cause vascular relaxation through blockade of adrenergic $\alpha$$\_$1/-receptors and some unknown mechanisms, and that there is some difference in sensitivity of vascular smooth muscle between NR and SHR in responses to ginseng saponins. It seems that panaxatriol type of some ginseng saponins has the greatest potency in vascular relaxation.

• Journal of Ginseng Research
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• v.19 no.2
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• pp.134-137
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• 1995

Ginseng saponins were analyzed by thermospray (TSP) LCMS method using ODS column and with acetonitrile/ammonium acetate solution. Optimal condition for TSP Lchfs was found as follows: capillary temperature: 33$0^{\circ}C$ repelled voltage: 200 V, and concentration of ammonium acetate: 0. 05 M. Panaxadiol and panaxatriol type saponins showed characteristic fragment ions. The calibration curve of ginseng saponin showed good linearity with a correlation coefficient of 0.99. Detection limits using selected ion monitoring (SIM) technique were improved by 10~200 times compared to conventional HPLCnnr detection method.