Endothelin-1 inhibition of the ATP-sensitive K+ channel in guinea-pig ventricular cardiomyocytes.
1. Effects of endothelin-1 on the ATP-sensitive K+ channel were examined in guinea-pig ventricular cardiomyocytes. 2. The ATP-sensitive K+ channel was activated outwardly with amplitude of about 2.2 pA at 0 mV. The conductance was 31 pS at 5.4 mM external K+ solution. The open probability was inhibited, and was completely blocked at 1 nM of endothelin-1. 3. In contrast, endothelin-3 (1 nM) did not cause any effects on the channels. 4. Endothelin-1 (10 nM) significantly prolonged the action potential duration. These responses were reversible. 5. These results suggest that endothelin-1 may reverse the physiological responses to the stimulation of ATP-sensitive K+ channels, indicating its regulatory mechanisms under the disease conditions.
Satoh
H
H
Department of Pharmacology, Nara Medical University, Kashihara, Japan.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D016232:Endothelins / Q000378:metabolism*; D005905:Glyburide / Q000494:pharmacology; D006168:Guinea Pigs; D006321:Heart / Q000187:drug effects*; D006352:Heart Ventricles / Q000166:cytology / Q000187:drug effects; D007004:Hypoglycemic Agents / Q000494:pharmacology; D015221:Potassium Channels / Q000187:drug effects*
D016232:Endothelins; D007004:Hypoglycemic Agents; D015221:Potassium Channels; D005905:Glyburide