가토 대동맥 평활근에서 인삼 알콜 추출물에 의한 Calcium 동원에 관한 연구

A Study on the Mobilization of Calcium by Ginseng Alcohol Extract in Rabbit Vascular Smooth Muscle

There have been conflicting reports concerning the effect of Panax ginseng on the contractility of vascular smooth muscle, i.e., Panax ginseng extract has been reported to cause relaxation, contraction or to have no effect on the tension of vascular smooth muscle. A further investigation of Ca⁺⁺ stores which supply Ca⁺⁺ for contraction of vascular smooth muscle is needed to understand the underlying mechanisms of this conflicting effect of ginseng alcohol extract (GAE). The present study was intended to examine the sources of calcium mobilized for contraction of vascular smooth muscle by GAE. Aortic ring preparations were made from the rabbit thoracic aorta and endothelial cells were removed from the ring. The contractility of the aortic ring was measured under various experimental conditions and Ca⁺⁺ flux across the membrane of aortic ring and the sarcoplasmic reticulum and mitochondria were measured with a calcium selective electrode. The result were summarized as follows; 1) At low concentration of extracellular Ca⁺⁺, GAE increased the contractility of vascular smooth muscle in dose-dependent fashion except high concentration Ca⁺⁺ (1 mM). 2) In the presence of ryanodine, GAE still increased contractility of vascular smooth muscle as much as control group, but in the presence of caffeine, GAE increased it significantly. i.e. Their effects seemed to be additive. 3) In the presence of verapamil+lanthanum, and verapamil+lanthanum+ryanodine, the contractility of the vascular smooth muscle was decreased, but a dose dependent increase in vascular tension was still demonstrated by GAE although total tension was low. 4) GAE increased Ca⁺⁺ efflux from vascular smooth muscle cells, but have no effect on Ca⁺⁺ influx. 5) GAE increased Ca⁺⁺ efflux from sarcoplasmic reticulum and mitochondria vesicles. From the above results, it may be concluded that GAE increased the release of Ca⁺⁺ from sarcoplasmic reticulum, mitochondria or other intracellular Ca⁺⁺ stores of vascular smooth muscle, but it does not increase Ca⁺⁺ influx across the plasma membrane.