ATP Directly Affects Junctional Conductance Between Paired Ventricular Myocytes Isolated From Guinea Pig Heart

• Published in: Circulation research Vol. 66; no. 4; pp. 1095 - 1102
• Main Authors: Sugiura, Hiroki, Toyama, Junji, Tsuboi, Naoya, Kamiya, Kaichiro, Kodama, Itsuo
• Format: Journal Article
• Language: English
• Published: Hagerstown, MD American Heart Association, Inc 01.04.1990; Lippincott
• Subjects: Adenosine Diphosphate - pharmacology; Adenosine Triphosphate - pharmacology; Adenylyl Imidodiphosphate - pharmacology; Animals; Biological and medical sciences; Cell Separation; Colforsin - pharmacology; Cyclic AMP - pharmacology; Electric Conductivity; Fundamental and applied biological sciences. Psychology; Heart; Heart Ventricles; Intercellular Junctions - physiology; Myocardium - cytology; Myocardium - ultrastructure; Osmolar Concentration; Temperature; Vertebrates: cardiovascular system; Heart; Rodentia; Electrophysiology; Heart ventricle; In vitro; Gap junction; Voltage clamp method; Myocyte; Vertebrata; Mammalia; Guinea pig; Circulatory system; ATP
• ISSN: 0009-7330; 1524-4571
• DOI: 10.1161/01.res.66.4.1095

Effects of ATP on junctional conductance (gj) were investigated in paired ventricular myocytes isolated from guinea pig hearts. One cell of the pair was voltage-clamped with a single-patch pipette, and gj was measured after the perforation of the nonjunctional membrane of the partner cell. The current-voltage relation of gj was linear between −30 and +30 mV. The control gj at 5.0 mM ATP in 88 pairs of cells ranged from 100 to 1,055 nS (average, 268 nS). ATP within the range from 0.1 to 5.0 mM increased gj in a dose-dependent manner. The Hill coefficient was 2.6, and the half-maximum effective concentration of ATP was 0.68 mM. Adenylylimidodiphosphate (2 mM) caused a transient increase in gj in the presence of 0.5 mM ATP, but forskolin (30 μM), cyclic AMP (50 μM), catalytic subunit of cyclic AMP-dependent protein kinase (1 μM), and ADP (10 mM) had no significant effect on gj. The temperature coefficient of gj in the presence of 5.0 mM ATP was 1.29. These findings suggest that gj in paired ventricular myocytes is directly regulated by ATP probably through a specific ligand-receptor interaction between ATP and gap junctional channel protein.