Effects of Endothelium-derived Relaxing Factors on the Regulation of ATP-sensitive Potassium Channel Activity in Cardiac Myocytes.
10.4070/kcj.2003.33.5.420
- Author:
Jeong Min JU
1
;
Dong Ho SHIN
;
Han Seong JEONG
;
Hyung Wook PARK
;
Jeong Gwan CHO
;
Jae Ha KIM
Author Information
1. Department of Pharmacology, Chonnam National University Medical School, Gwangju, Korea. kimjh@chonnam.ac.kr
- Publication Type:Original Article
- Keywords:
ATP-sensitive potassium channel;
Myocytes cardiac;
Endothelium-derived relaxing factor;
Patch clamp techniques
- MeSH:
Adenosine Diphosphate;
Adenosine Triphosphate;
Animals;
Baths;
Endothelium-Dependent Relaxing Factors*;
Epoprostenol;
Humans;
Mice;
Muscle Cells;
Myocytes, Cardiac*;
Nitric Oxide;
Patch-Clamp Techniques;
Potassium Channels*;
Potassium*;
Spermine;
Tissue Donors
- From:Korean Circulation Journal
2003;33(5):420-430
- CountryRepublic of Korea
- Language:Korean
-
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.
