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摘要
Aim To investigate the role of Ca2+sensor STIM1 in mouse aortic smooth muscle contractile response. Methods Smooth muscle-targeted STIM1-knockout (sm-STIMl-KO) mouse was generated by cre-lox technology. The changes of the response to different vasoconstrictors were measured in mouse aorta using a Multi Myograph System. And different Ca channel blockers were given to observe the changes of vasoconstriction. Results The sm-STIMl-KO mice were successfully prepared. Store-operated calcium channel (SOCC)-mediated vasoconstriction disappeared in sm-STIMl-KO mice. Compared with wildtype mice, sm-STIMl-KO mice showed no significant changes in response to Phe, 5-HT and U46619. In the K-H solution with and without Ca2+, vasoconstriction of both groups was inhibited after nifedipine incubation, and vasoconstriction of sm-STIMl-KO was lower than that of wild-type mice (P < 0. 01). In a 60 mmol · L-1KC1 solution containing nifedipine, the fast phase contraction induced by Phe did not change, but the slow phase contraction decreased significantly (P < 0.01). In sm-STIMl-KO mice, peak-reaching and descending rates of vasoconstriction mediated by Ca2+release from sarcoplasmic reticulum were accelerated (P <0. 05). Conclusions STIM1 is an essential component of SOCC-mediated vasoconstriction and is involved in SOCC and sarcoplasmic reticulum Ca2+release-mediated vasoconstriction. ? 2021 Publication Centre of Anhui Medical University.
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