[Changes of ERK1/2 in femoral arteries of tail-suspended rats and their effects on contractility].

OBJECTIVE

To study changes of extracellular signal-regulated kinase 1 and 2 (ERK1/2) in femoral arteries of tail-suspended rats and their effects on contractility.

METHOD

Microgravity was simulated by elevating the hindquarters of Wistar rats to produce hindlimb unweighting (HU). In the absence or presence of prazosin and PD98059 respectively, isometric tension of vessel rings from femoral arteries in response to norepinephrine (NE) was determined by in vitro perfusion technique; Basal total ERK1/2 level and phosphorylated ERK1/2 level stimulated by norepinephrine in the absence or presence of prazosin and PD98059 respectively were detected by Western blotting-enhanced chemically lightening system.

RESULT

The maximal contractile response to NE was significantly lower in femoral arterial rings from 14 day-HU rats as compared with those in control rats. PD98059 caused a marked inhibition of NE-induced maximum contractile response in both control and HU femoral arterial rings. Moreover, the effect of inhibition was more significant in control rats than that in HU rats. Prazosin caused a right shift of the concentration-response curves (CRCs) to NE in both control and HU rats, but no difference was found between the two groups for the PA2 of prazosin calculated by Schild analysis, which showed that the sensitivity of alpha1 adrenoceptor was not changed by HU. After 7d-recovery, the difference of contractile response of femoral arterial rings to NE between recovered group and control group was nonsignificant. Data from Western blotting showed that basal total ERK1/2 levels were elevated in femoral arterial rings from 14d-HU rats as compared with those in control rats, but the levels of basal and NE-stimulated phosphorylated ERK1/2 were higher in control as compared with HU rats. After 7d recovery, the basal total ERK1/2 level and phosphorylated ERK1/2 level were not different from control.

CONCLUSION

Microgravity simulated by 14d-HU can induce abnormality of MAPK/ERK pathway, which may contribute to declined contractile response of femoral vessel rings to NE.