Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we will assume that you are happy to receive all cookies and you will not see this message again. Click 'Find out more' for information on how to change your cookie settings.

Although protons can directly or indirectly gate solute permeability of the myocardial gap junction, there is little information regarding their own permeation, despite their importance in the regulation of myocardial contractility and rhythm. By pipette-loading of acid into guinea pig isolated, ventricular myocyte pairs while imaging pH(i) confocally using SNARF fluorescence, we have observed that protons permeate the junctional region. Permeation is inhibited by glycyrrhetinic acid, an agent that also increases intercellular electrical resistance, suggesting H+ permeation via gap junctions. The rate of spread of acid between cells appears to be limited by junctional permeation rather than by cytoplasmic diffusion. Mathematical analyses, combined with experiments using SNARF as a proton carrier, suggest that gap junctional H+ transmission may be accomplished physiologically by the permeation of intrinsic "proton-porter" molecules. We propose that proton flux through gap junctions will contribute to the dissipation of regional acid loads within the myocardium. This represents a mechanism for the local control of myocardial pH(i).

Original publication

DOI

10.1161/01.RES.0000093986.47383.CE

Type

Journal article

Journal

Circ Res

Publication Date

17/10/2003

Volume

93

Pages

726 - 735

Keywords

Animals, Benzopyrans, Cell Membrane Permeability, Cells, Cultured, Electric Impedance, Fluorescent Dyes, Gap Junctions, Glycyrrhetinic Acid, Guinea Pigs, Hydrogen-Ion Concentration, Ion Channel Gating, Ion Transport, Kinetics, Microscopy, Confocal, Models, Biological, Myocardium, Myocytes, Cardiac, Naphthols, Proton Pumps, Protons, Rhodamines, Sarcolemma