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  • Title: The vasorelaxant effect of antidiabetic drug nateglinide via activation of voltage-dependent K+ channels in aortic smooth muscle.
    Author: Li H, Kim HW, Shin SE, Seo MS, An JR, Jung WK, Ha KS, Han ET, Hong SH, Bang H, Choi IW, Na SH, Park WS.
    Journal: Cardiovasc Ther; 2018 Feb; 36(1):. PubMed ID: 28834298.
    Abstract:
    AIMS: We investigated the vasorelaxant effect of nateglinide and its related mechanisms using phenylephrine (Phe)-induced precontracted aortic rings. METHODS: Arterial tone measurement was performed in aortic smooth muscle. RESULTS: The application of nateglinide induced vasorelaxation in a concentration-dependent manner. Pretreatment with the large-conductance Ca2+ -activated K+ (BKCa ) channel inhibitor paxilline, the inwardly rectifying K+ (Kir) channel inhibitor Ba2+ , and ATP-sensitive K+ (KATP ) channel inhibitor glibenclamide did not affect the vasorelaxant effect of nateglinide. However, pretreatment with the voltage-dependent K+ (Kv) channel inhibitor 4-aminopyridine (4-AP) effectively reduced the vasorelaxant effect of nateglinide. Pretreatment with the Ca2+ inhibitor nifedipine and the sarcoplasmic/endoplasmic reticulum Ca2+ -ATPase inhibitor thapsigargin did not change the vasorelaxant effect of nateglinide. Additionally, the vasorelaxant effect of nateglinide was not altered in the presence of an adenylyl cyclase, a protein kinase A, a guanylyl cyclase, or a protein kinase G inhibitor. The vasorelaxant effect of nateglinide was not affected by the elimination of the endothelium. In addition, pretreatment with a nitric oxide synthase inhibitor, L-NAME, and a small-conductance Ca2+ -activated K+ (SKCa ) channel inhibitor, apamin, did not change the vasorelaxant effect of nateglinide. CONCLUSION: Nateglinide induced vasorelaxation via the activation of the Kv channel independent of other K+ channels, Ca2+ channels, intracellular Ca2+ ([Ca2+ ]i ), and the endothelium.
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