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Testosterone-Enhances-KV-Currents-and-Airway-Smooth-Muscle-Relaxation-Induced-by-ATP-and-UTP-through-P2Y4-Receptors-and-Adenylyl-Cyclase-Pathway-PMC.md

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However, exposure to TES increased the contribution of KV channels (69.86%) but decreased that of BKCa channels (30.13%) (Figure 6B). Notably, 4-AP completely blocked the TES-induced enhancement of K+ currents, highlighting the importance of KV channels in this phenomenon. As shown in Figure 4A and Figure 5A, ATP- and UTP-induced K+ currents in control myocytes (without TES) were partially decreased by 4-AP, and the remaining K+ currents were abolished by the addition of IBTX. The major populations of K+ channels involved in the modulation of the tone and relaxation of the ASM are the KV and BKCa 27,40,56,58,69. To confirm the possible genomic mechanism of TES, we used flutamide, [http://47.104.60.158/](http://47.104.60.158:7777/samiradeegan0) an androgen receptor antagonist, which abolished the sex-hormone-induced effects on the K+ currents (Figure 2 and Figure 3).
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For example, androgens induce the relaxation of pre-contracted guinea pigs and bovine tracheal smooth muscle by blocking L-type voltage-dependent Ca2+ channels (L-VDCCs) and store-operated Ca2+ channels (SOCCs) 51,52. These previous results suggest that the higher relaxation induced by ATP than UTP may be mediated by adenosine acting through P1 receptors . Moreover, we also showed a remanent relaxation induced by ATP even when P2Y2 and P2Y4 receptors were blocked .
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