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Differential Vascular Effects of Panax Ginseng and Panax Quinquefolius Extracts

Contact Person: C. Y. Kwan (kwancy@fhs.mcmaster.ca)


Effect of Panax ginseng on vascular contractility

Effect on the resting tone

When 0.6 mg/ml of the standardized Panax ginseng extract G-115, was added to the organ bath containing endothelium-denuded aortic rings isolated from SHR and WKY, an inhibition of the resting tone was observed in SHR aorta, but not in WKY aorta. This finding suggests that G-115 interacted directly with the vascular smooth muscle cells and caused relaxation. We have also found that such a selective inhibition of the myogenic tone in SHR also occurred with the addition of 0.5 mM EGTA. The inhibitory action of G-115 in SHR is apparently associated with Ca2+ influx pathway.

Effect on Na+-induced contraction

Dysfunction of cellular response to sodium ion (Na+) has also been implicated in the pathogenesis of hypertension. Indeed, we have previously reported that in Mg2+- and Ca2+-deficient conditions, Na+ at even low concentrations produced a prominent contraction in rat aorta (Kravtsov and Kwan, 1995a), which was also found to be exaggerated in SHR compared to WKY (Kravtsov and Kwan, 1995b). This Na+-contraction was counteracted by reintroduction of physiological concentration of Mg2+. We observed that this Na+-induced contraction in rat aorta was also inhibited by 0.6 mg/ml G-115 and the inhibition was comparable to that induced by re-introduction of 2 mM Mg2+.

Effect on phenylephrine (PE)-induced contraction

Figure 3 shows the effect of addition of 0.6 mg/ml G-115 to the aortic ring preparations that were precontracted with various concentrations of PE. Low concentrations of PE (20-40 nM) produced transient contraction overlaid by rhythmic activities. A tonic phase was obtained at 60 nM PE and G-115 caused prominent inhibition of the tone. As the concentration of PE was increased to >0.3 uM, sustained contractions without the rhythmic activities were observed. However, the degree of inhibition by G-115 of this sustained PE-contraction was only partial at 0.3 uM PE and was almost absent at 3 uM PE, which caused maximal contraction. The inhibitory effects of G-115 (on the resting tension. PE-contraction and Na+-contraction) were totally reversible.

Effect on KCl-induced contraction

Hypertonically added KCl (60 mM) induced sustained contraction and, unlike PE-induced contraction, this contraction produced over a wide range of KCl concentration (20-100 mM) was not affected by the addition of 0.6 mg/ml G-115. We have previously observed (Guan et al., 1988; 1990)) that the extract of Panax notoginseng containing the total saponins also elicited similar effects as the standardized root extract (G-115) of the Panax ginseng.

Effect of Panax quiquefolium on vascular contractility

We also studied the effects of 0.5 mg/ml of leaf and stem saponins isolated from (PQS) Panax quinquefolius from a commercial source in China on the KCl-induced contraction of endothelium-denuded DCA ring preparations. Phentolamine (10 uM; a non-selective alpha-adrenoceptor antagonist) was also added to inhibit possible contraction that was generated due to norepinephrine release from the sympathetic nerve endings as a result of membrane depolarization induced by high KCl. We observed that 0.5 mg/ml PQS caused an inhibition by about 30% of phentoalamine-insensitive, KCl-induced contraction and this inhibition was readily reversible. The recovery of KCl contraction after an extensive washout of PQS was however not complete.

We have also examined the effects of PQS on PE-induced contraction. We observed that 0.5 mg/ml exerted a small (about 10%) apparent inhibition of the contractile response to cumulatively added PE. However, this inhibitory effect may be largely due to other unidentified adverse effects of PQS, since the washout of PQS did not totally restored PE-contraction, particularly at low concentrations of PE.

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Kwan, CY; (1998). Differential Vascular Effects of Panax Ginseng and Panax Quinquefolius Extracts. Presented at INABIS '98 - 5th Internet World Congress on Biomedical Sciences at McMaster University, Canada, Dec 7-16th. Invited Symposium. Available at URL http://www.mcmaster.ca/inabis98/kwan/kwan0249/index.html
© 1998 Author(s) Hold Copyright