Objective: To confirm the action of glycyrrhizin on blood pressure by inhibiting the activity of 11beta-hydroxysteroid dehydrogenase type II (11betaHSD 2) and to test its mechanism.
Methods: Male Wistar rats and SHRs (weighing 150 - 220 g) were given glycyrrhizin (Sigma) 200 mg/kg/day, orally for 5 weeks and 3 months. The blood pressure was monitored by means of a pressure transducer connected to a polygraph and recorded. Histological pathological changes of the nutrient arteries of the heart and aorta were studied with light microscope. Mesenteric artery perfusion ex vivo and pressor responses to norepinephrine were performed. The perfusate from the mesenteric arteries was collected and used for reverse phase high performance liquid chromatography to measure aldosterone and corticosterone level. RT-PCR was used to measure the expression of 11betaHSD 2 and aldosterone synthase (CYP11B2) mRNA.
Results: The results showed that the systolic blood pressure was significantly increased in Wistar rats treated with glycyrrhizin compared with those not treated. Hyperplasia of smooth muscle cells and hypertrophy in arterioles were observed under microscope. The pressor responses to norepinephrine in mesenteric arteries treated with glycyrrhizin were significantly increased. The level of aldosterone was decreased but that of corticosterone was increased in perfusate treated with glycyrrhizin. RT-PCR showed that glycyrrhizin inhibited the expression of 11beta-HSD2and CYP11B2 mRNA in aorta.
Conclusion: These results confirm that glycyrrhizin is able to induce hypertension. There is evidence that it inhibits the enzymes of both 11beta-HSD2 and CYP11B2 in vasculature and leads to higher corticosterone and lower aldosterone production in vessels as well as an increase in vascular responses to norepinephrine.