PULMONARY VASCULAR EFFECTS OF GINSENOSIDES

We reported earlier (Br. J. Pharmac. 82. 485 - 491. 1984) that ginsenosides from Panax ginseng CA. Meyer antagonized noradrenaline or prostaglandin $F_{2\alpha}-induced$ contractions of pulmonary and intrapulmonary arterial rings of rabbits. Because this effect resembled that of acetylcholine (ACh). we questioned whether these acitons were due to release of nitric oxide from vaseular endothelium. We therefore determined whether ginsenosides could vasodilate preconstricted lungs and also protect against free radical injury. which normally eliminates the vasodilator response to ACh(J. Appl. Physiol. 71. 821 - 825. 1991 J. We found that ginsenoside $Rg_1$ or a mixture of saponins could ,a) vasodilate perfused. $U_{46619}-preconstricted$ lungs. b) promote increased synthesis of nitric oxide by endothelial cells in culture and c) prevent the pulmonary edema often associated with free radical injury (Biochem. Biophys. Res. Comm. 189. 670 - 676. 1992). Thus, vasodilator and protective effects of ginsenosides against free radical injury may reflect enhanced synthesis and release of nitric oxide. These data suggest that ginsenosides may be useful in treatment of pulmonary and systemic hypertension. Aided by grants from the National Institutes of Health. Bethesda.