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Korean Circ J. 2006 Jul;36(7):516-525. Korean. Original Article.
Kim JH , Ju JM , Piao LH , Kim YY , Jeong HS , Park HW , Jeong DH , Lee SR , Yoon NS , Kim KH , Hong YJ , Kim JH , Kim W , Ahn YK , Jeong MH , Cho JG , Park JC , Kang JC .
Department of Pharmacology, Chonnam National University Medical School, Gwangju, Korea.
Department of Physiology, Chonnam National University Medical School, Gwangju, Korea.
Department of Cardiovascular Medicine, Chonnam National University Medical School, Gwangju, Korea.

BACKGROUND AND OBJECTIVES: It has been known that various vasoactive agents are involved in the regulation of cardiac function through the modification of the K+ channel activities, including the ATP-sensitive K+ channel (KATP). We examined the effects of several vasoactive agents on the cardiac KATP currents in isolated cardiac myocytes. MATERIALS AND METHODS: Ventricular myocytes were isolated from the hearts of ICR mice by enzymatic digestion. The channel currents were recorded by the excised inside-out and cell-attached patch clamp configurations. RESULTS: In the excised inside-out patches, bradykinin (BRK; 1-10 micrometer) and prostaglandin I2 (PGI; 10-50 micrometer) did not affect the channel activities, whereas the vasodilators increased the attenuated channel activities in the presence of 100 micrometer ATP. BRK and PGI in parallel shifted the dose-response curves of ATP (1-1,000 micrometer), and this inhibited the KATP currents to the right. Endothelin (ET-1; 0.1-1 nM) and leukotriene D4 (LTD; 3-10 micrometer) decreased the channel activities immediately after making the inside-out patches. However, the vasoconstrictors did not affect the attenuated channel activities by ATP. In the cell-attached patches, both BRK and PGI increased the channel activities and these effects were markedly attenuated by glibenclamide (50 micrometer). ET-1 and LTD did not affect the baseline channel activities in the cell-attached patches, but they markedly attenuated the dinitrophenol-induced activities. CONCLUSION: It was inferred that certain vasoactive substances are involved in the regulation of cardiac KATP channel activities, and that bradykinin and PGI2 enhance the channel activities, and ET-1 and LTD4 inhibit the channel activities.

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