Differential Expression Of Gap Junction In Spontaneously Hypertensive And Normotensive Rat Aorta

Objective: To investigate the expression of connexins in aorta of the spontaneously hypertensive rats(SHR) and normotensive rats.Methods: We investigated the difference of Cx37, Cx40, Cx43 and Cx45 mRNA and protein expression between SHR and normotensive rats aorta by quantitative RT-PCR and Werstern-blot respectively, and detected the morphological change of gap junction between smooth muscle cells by transmission electron microscopy.Results:(1) The expression of Cx37, Cx40 and Cx43 and Cx45 m RNA results by RT-PCR in SHR and normotensive Wistar rats show: compared with normotensive Wistar rats the expression of Cx37 to SHR in aortic is decreased, with statistical significance(P<0.01); compared with normotensive Wistar rats the expression of Cx40 to SHR have no statistical significance(P>0.05); compared with normotensive Wistar rats the expression of Cx43 and Cx45 to SHR is reduced with statistically significant(P<0.05), but more significantly in Cx43(P<0.01).That Rt-pcr detection of blood pressure of SHR and normal rat aortic normal blood pressure(2) The expression of Cx37, Cx40 and Cx43 and Cx45 results by Western blot in SHR and normotensive Wistar rats show: Compared with normotensive Wistar rats the expression of Cx37 to SHR in aortic is decreased, with statistical significance(P<0.01); Compared with normotensive Wistar rats the expression of Cx40 to SHR have no statistical significance(P>0.05). The aortic Cx43 and Cx45 protein of SHR were significantly decreased compared with the normotensive rats by Western blot(P<0.01). The level of phosphorylated Cx43 is higher in SHR, but no differente to Wistar rat in aorta(P>0.05).(3) The number of gap junctions between smooth muscle cells was significantly lower in SHR than in normotensive rats. Between smooth muscle cells,SHR have more white collagen than normotensive rats.Conclusion: Hypertension could down-regulate the expression of Cx43 and Cx45 and decrease the number of gap junction between aortic smooth muscle cells to make vascular function disorders, further aggravating the damage induced by hypertension.