The Effect Of18β-GA Contraction On Activities Cerebrovascular And The Expressions Of Connexins In SHR And Wistar Rats

Object：To investigate the effects of18β-glycyrrhetinic acid(gap junction blockers) on the cerebral arterycontraction and relaxation activities, and to compare the Connexins expression of cerebral artery betweenspontaneously hypertensive rats (SHR) and Wistar rats. To provide some new ideas for the clinical treatment ofhypertension correlation cerebrovascular disease.Methods: Pressure myograph was used to observe the influences of KCl and PE on the vascular contractionactivities, and to observe the influences of SNP on the vasodilatation, after applying18β-GA. The expressions ofconnexin(Cx) in the brain vascular tissue were examined by Western blotting.Results:(1)KCl induced the MCAcontraction in a concentration-dependent manner both SHR and Wistarrats;and their the contraction amplitudes of MCAwas obviously suppressed by KCl, while after pretreated by18β-GA(100μmol/L). In SHR, the inhibitory percent of KCl(80mmol/L) decreased from95%±9%to63%±8%, statistically significant difference (P <0.05, n=6),In Wistar rats, the inhibitory percent of KCl(80mmol/L)decreased from100%±8%to64%±6%, statistically significant difference (P <0.05, n=6), Compared with theWistar rats, the dose-effect curve of KCl shift to the left in SHR, and contration of KCl(10~30mmol/L) increasedsensitivity in SHR. Vessels incubated with18β-GA(100μmol/L), Respectively, EC50of KCl were23.99mmol/Land32.62mmol/L in SHR(P﹥0.05, n=6), EC50of KCl were36.96mmol/Land34.90mmol/L in Wistarrats (P﹥0.05, n=6).PE induced the MCAcontraction in a concentration-dependent manner both SHR and Wistar rats;thecontraction amplitudes of MCAwas obviously suppressed by PE, while after pretreated by18β-GA(100μmol/L).the inhibitory percent of PE(100μmol/L) decreased from237%±30%to91%±3%in SHR; the inhibitorypercent of PE(100μmol/L) decreased from100%±11%to40%±8%in Wistar rats, statistically significantdifference (P <0.01, n=6).Respectively, EC50of PE were11.29μmol/L and0.86μmol/L in SHR(P﹥0.05,n=6), EC50of PE were0.46μmol/L and5.60μmol/L in Wistar rats (P﹥0.05, n=6).SNP induced the MCArelaxation in a concentration-dependent manner both SHR and Wistar rats. theinhibitory effects of18β-GA (100μmol/L) were significantly greater in SHR, In SHR, the inhibitory percent ofSNP(300μmol/L)decreased from91%±13%to57%±8%(P <0.05, n=6);In Wistar rats, the inhibitory percent ofSNP(300μmol/L)decreased from100%±7%to61%±10%(P <0.05,n=6). Respectively, EC50of SNP were2.12μmol/L and6.24μmol/L in SHR(P﹥0.05, n=6). EC50of SNP were2.56μmol/L and1.51μmol/Lin Wistar rats (P﹥0.05,n=6). (2)Compared with the Wistar rats, western blot demonstrated that the expression of Cx43and Cx45wasgreater in SHR, but the expression of Cx43was lower in SHR(P <0.05,n=6).Conclusion:18β-GAmight the contraction of MCA; and gap junction blockers can significantly inhibit theactivities of cerebrovascular contraction and relaxation; the Connexins expression was changed incerebrovascular.