Korean Circulation Journal 2003;33(5):420-430
doi:10.4070/kcj.2003.33.5.420
Effects of Endothelium-derived Relaxing Factors on the Regulation of ATP-sensitive Potassium Channel Activity in Cardiac Myocytes.
Jeong Min JU 1 ; Dong Ho SHIN ; Han Seong JEONG ; Hyung Wook PARK ; Jeong Gwan CHO ; Jae Ha KIM
Affiliations
Keywords
ATP-sensitive potassium channel; Myocytes cardiac; Endothelium-derived relaxing factor; Patch clamp techniques
Country
Republic of Korea
Language
Korean
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Abstract
BACKGROUND AND OBJECTIVES: Effects of the three major endothelium-derived relaxing factors (EDRFs), namely nitric oxide (NO), prostacyclin (PGI2), and 11, 12-epoxyeicosatrienoic acid (EET) on the ATP-sensitive potassium channel (K ATP channel) activity were examined in isolated cardiac ventricular myocytes. MATERIALS AND METHODS: K ATP channel activities were measured in the enzymatically (collagenase) isolated single mouse ventricular myocytes using excised inside-out, cell-attached, and perforated whole-cell patch clamp techniques. RESULTS: In inside-out patches, NO donors, SNP and spermine NONOate, did not affect the K ATP channel activity. In the presence of both ATP and ADP in the bath solution, the NO donors attenuated the activity of the K ATP channel. In cell-attached patches, the NO donors potentiated pinacidil-induced K ATP channel activity. In perforated whole-cell patch configuration, the NO donors decreased the K ATP current induced by PCO 400, a K ATP channel opener. PGI2 did not affect the K ATP channel activity in excised insideout patch. However, in the pres-ence of ATP in the internal solution, PGI2 increased the channel activity in a dose-dependent manner. In cell-attached patches, PGI2 did not only affect the channel activity itself, but also the dinitrophenol-induced K ATP channel activity. 11, 12-EET had no effect on K ATP channel activities.CONCLUSION: These results indicate that some of the endothelium-derived relaxing factors (nitric oxide and prostacyclin) are involved in the regulation of ATP-sensitive potassium channel activities in mouse ventricular myocytes; and the regulation type was com-plicated, activation or inhibition, depending on the cellular environment.
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