Objective   To investigate the effect of the expression of voltage-gated K

+

channel Kv2.1 in the development and regression of pulmonary arterial hypertension (PAH) in hypobaria and hypoxia rats.   Methods   Totally 32 adult male Sprague-Dawley rats (200 to 250 g) were randomly and equally divided into 4 groups

normal group (N group)

ch

ronic hypoxia group (CH group)

Dichloroacetate (DCA

70 mg·kg

-1

·d

-1

introgastrically) treated group (CH+DCA group)

and chronic hypoxia return to normal conditions for 7 d group (CHR

7

group). For the rats of the CH

CH+DCA and CHR

7

groups

5 000 meter high altitude circumstance was simulated by exposure rats in a hypobaric and hypoxia chamber for 21 d. Rats in N group were fed in normal air pressure and PO

2

conditions. The animals of N

CH and CH+DCA groups were sacrificed for mPAP measurement and tissue harvest at day 21. The mPAP measurement and tissue harvest of CHR

7

group were performed after the rats returned to normal conditions for 7 d. Real time PCR

immunohistochemical staining and Western blot analysis were carried out to detect the Kv2.1 expression in pulmonary arterial smooth muscle cells (PASMCs).   Results   Compared with the rats in N group

the mRNA and protein expressions of Kv2.1 in the PASMCs in CH rats were deceased but mPAP were increased significantly

and the pulmonary artery wall were thickened significantly. However

compared with the CH rats

the Kv2.1 mRNA and protein expressions of the CH+DCA group and CHR

7

group were restored and mPAP were decreased

and the pulmonary artery wall thicken was slightly.   Conclusion   The expression of Kv2.1 is negatively correlated with the chronic hypoxia hypertension

suggesting that Kv2.1 may play an important role in the development and regression of PAH.