Abstract

The present study tested the hypothesis that the role of ERK in phasic and tonic contractile responses is declined by hindlimb unloading (HU) in rat femoral arteries. Male Wistar rats were randomised into HU and Control group (n=7). After 14d, the femoral arteries were isolated and cut into 3-mm ring segments. In the absence or presence of PD98059(MEK inhibitor), contractile response to NE(10μM) was measured in Krebs solution in a tissue bath at 37°C, isometric tension were recorded with Powerlab system. The area under curve (AUC), phasic and tonic contractile responses between two groups were compared. After 14d-HU, the AUC, phasic and tonic NE-induced contractile responses were declined compared with controls. PD98059 did not affect the AUC in arteries from HU, but significantly decreased the AUC in arteries from control (100±7.1% vs. 61.18±11.3%, P<0.05). In contrast to control, the inhibitory ratio of PD98059 was significantly lower in phasic (7.42±3.24% vs. 33.59± 9.19%, P=0.0198) and tonic (26.93±3.78% vs. 46.75±5.67%, P=0.0131) contractile responses of HU group. Moreover, the inhibitory ratio of PD98059 wasn't significantly different between the phasic and tonic contractile responses in control group (P=0.2464). But for HU group, the difference was statistically significant (P=0.002). We demonstrated that the role of ERK was declined in both phasic and tonic contractile responses in rat femoral arteries after hindlimb unloading. Simulated microgravity induced by HU may attenuate the contractile responses of femoral arteries by inhibiting the role of ERK in thick and thin filament regulatory pathways.

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