ANTIHYPERTENSIVE EFFECTS OF TOTAL GINSENOSIDES AND REGULATION OF THE PERTURBED METABOLISM OF SPONTANEOUSLY HYPERTENSIVE RATS

Essential hypertension is inherently associated with metabolic disorders, and its pathogenesis remains poorly understood. Analyses of the metabolic perturbation of hypertension and the regulation of this perturbed metabolism using therapeutic agents can extend our insight into the pathogenesis of this disease. We used gas chromatography mass spectrometry and principal component analysis to profile the metabolic phenotype of hypertension in spontaneously hypertensive rats (SHR) and studied the regulatory effect of total ginsenosides (TG) and four typical antihypertensive agents on in vivo metabolism. The five agents yielded different hypotensive effects and distinct regulation patterns on the perturbed metabolism that occurs in SHR. Captopril, amlodipine, and terazosin efficiently depressed systolic blood pressure (SP) but had a negligible regulatory effect on the perturbed metabolism of SHR, even after the remission of hypertension for 8 weeks. In contrast, TG gradually and markedly regulated the perturbed metabolism, and led to a mild but sustained depression of SP up to 2 weeks after the cessation of treatment. Remarkably, TG downregulated free fatty acids (FFA) toward normal levels; the elevation of FFA correlates with blood pressure, in both animals and humans. These results suggest that TG may act as a special antihypertensive agent that regulates the perturbed metabolism of hypertension.