고려홍삼은 혈압강하효과가 있음이 잘 알려져 있다. 이에 백서장간막이 동맥의 저항혈관에서 고려홍삼 사포닌 성분의 혈관 이완기전을 규명하고자 내경이 150$mu extrm{m}$이하의 작은 혈관을 이요하여 여러 실험 조건에서 장력의 변화를 측정하여 다음과 같은 결과를 얻었다. 고려홍삼 사포닌 성분은 농도 의존적으로 (0.01mg/$mell$~1mg/$mell$) 혈관 평활근을 이완시켰으며 내피세포를 제거한 상태에서도 혈관의 이완효과는 지속되었다. A23187 이나 phorbol 12, 13-dibutyrate 에 의한 수축에서는 고려홍삼 사포닌에 의한 혈관의 이완효과가 나타나지 않았다. 고려홍삼 사포닌에 의한 혈관이완효과는 실험용액의 $K^{+}$ 농도를 증가시키면 감소되었으며 각종 $K^{+}$이 온통로 억제제인 tetaethylammonium, glybenclamide, 4-aminopyridine 및 BaCl$_2$를 전처치한 결과 BaCl$_2$에 의해서만 농도에 의존적으로 고려홍삼 사포닌에 의한 혈관이완작용이 억제되었다. 이상의 실험결과로부터 고려홍삼 사포닌은 장간막 동맥의 저항혈관에서 $K^{+}$의 유출을 증가시켜 혈관평활근을 이완시키며 $Ba^{2+}$에 의하여 차단되는 $K^{+}$ 이온통로가 고려홍삼 사포닌에 의한 혈관이완작용에 관여함을 알 수 있었다.
It has been well known that Korea red ginseng has an antihypertensive effect. The antihypertensive effect may be due to its ability to change the peripheral resistance. Change of vascular tone in the resistance-sized artery contribute to the peripheral resistance, thereby regulate the blood pressure. Therefore, we investigated to clarify the vasorelaxing mechanism induced by crude saponin of Korea red ginseng in the resistance-sized mesenteric artery of rats. The resistance-sized mesenteric artery was isolated and cut into a ring. The ring segment was immersed in HEPES-buffered solution and its isometric tension was measured using myograph force-displacement transducer. Crude saponin of ginseng relaxed the mesenmetric arterial rings precontracted with norepinephrine (3$mu$M) in dose-dependent manner (0.01 mg/㎖ -1 mg/㎖. The relaxation by crude saponin was smaller in endothelium-intact preparation than that in endothelium-denuded preparation. The contraction induced by A23187 or phorbol 12,13-dibutyrate was not affected by crude saponin of ginseng. The vasorelaxing effect of crude saponin of ginseng was significantly attenuated by the increase of the extracellular K$^$+/ concentration. Crude saponin-induced vasorelaxation was not affected by tetraethylammonium (1 mM), glybenclamide (10$mu$M), and 4-aminopyridine (0.1 mM) in these preparations. Ba$^$2+/(10$mu$M ∼100$mu$M) markedly reduced the crude saponin-induced vasorelakation dose-dependently. From the above results, we suggest that crude saponin of ginseng may stimulate K$^$+/ efflux and hyperpolarize the membrane, thereby cause the vasorelaxation in the resistance-sized mesenteric artery of rats.
