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目的:观察生理浓度睾酮短时作用对前列腺素F2α(PGF2α)诱导血管平滑肌细胞(VSMCs)中Ca2+升高的影响。方法:贴块法培养雄性SD大鼠胸主动脉VSMCs,钙敏荧光指示剂Fura-2负载细胞,Nikon TE-2000E活细胞工作站对VSMCs内钙信号进行测定。结果:VSMCs给以单纯PGF2α(10μmol/L)刺激,[Ca2+]i在数秒钟内由基线水平100nmol/L左右迅速升至约500nmol/L的峰值,随后呈缓慢下降,约150s降至基线水平。在PGF2α作用的峰值给以生理浓度(40nmol/L)睾酮或乙醇溶媒干预,前者能够明显缩短[Ca2+]i由峰值回落至基线水平的时间[与乙醇溶媒相比,(104.9±27.0)svs(153.5±40.4)s,P<0.01]。在PGF2α作用前预先给以睾酮或乙醇溶媒处理2min,前者对PGF2α刺激的[Ca2+]i峰值水平无明显影响[与乙醇溶媒相比,(390.0±126.0)nmol/Lvs(403.4±160.7)nmol/L,P>0.05],但使[Ca2+]i由峰值降至基线水平的时间显著缩短[与乙醇溶媒相比,(120.6±32.0)svs(151.4±27.4)s,P<0.01]。结论:睾酮对PGF2α诱导的VSMCs中[Ca2+]i升高具有快速抑制作用,提示睾酮通过与VSMCs细胞膜作用抑制受体门控钙通道介导的Ca2+内流。
Objective: To observe the effect of short-term physiological testosterone on the increase of Ca2 + in vascular smooth muscle cells (VSMCs) induced by prostaglandin F2α (PGF2α). Methods: VSMCs in thoracic aorta and Fura-2 loaded calcium sensitive indicator were cultured by patch method. Calcium signal in VSMCs was measured by Nikon TE-2000E living cell workstation. Results: VSMCs were stimulated with PGF2α (10μmol / L), and the number of [Ca2 +] i increased rapidly from baseline to 100nmol / L within a few seconds to a peak of about 500nmol / L, then decreased slowly and dropped to baseline at about 150s . The peak effect of PGF2α was given at a physiological concentration (40 nmol / L) of testosterone or ethanol vehicle, which significantly shortened the [Ca2 +] i peak from baseline to baseline levels (104.9 ± 27.0 vs svs 153.5 ± 40.4) s, P <0.01]. Pretreatment with testosterone or ethanol for 2 min before PGF2α administration showed no significant effect on peak levels of [Ca2 +] i stimulated by PGF2α [(390.0 ± 126.0) nmol / L vs (403.4 ± 160.7) nmol / L, P> 0.05], but the time to peak [Ca2 +] i was significantly reduced from baseline to baseline (120.6 ± 32.0 vs svs (151.4 ± 27.4) s, P <0.01 compared with vehicle vehicle). CONCLUSION: Testosterone has a rapid inhibitory effect on the increase of [Ca2 +] i in VSMCs induced by PGF2α, suggesting that testosterone inhibits Ca2 + influx mediated by receptor-gated calcium channel through the action of cell membrane of VSMCs.