title: Comparison of the effects of internal [Mg2+] on IK1 in cat and guinea-pig cardiac ventricular myocytes.
abstract: The effects of internal Mg2+ (Mg2+i) on processes underlying the inward rectification of the cardiac IK1 in enzymatically isolated cardiac ventricular myocytes (CVM) obtained from cat, guinea pig and rabbit were compared using the whole-cell and excised inside-out patch configurations of the voltage-clamp technique. In confirmation of the findings of other investigators, Mg(2+)i-sensitive outward IK1 currents could be elicited from guinea pig CVM at 15 degrees C when Mg2+i was reduced from 1 mM to less than 1 microM, suggesting that Mg2+i has an important role in the inward rectification of IK1 in guinea pig CVM at unphysiologically low temperatures. However, as temperature was raised to more physiological levels (e.g., 30 degrees C), Mg(2+)i-sensitive outward IK1 currents could no longer be evoked. In contrast with the results obtained with guinea pig CVM, IK1 remained inwardly rectifying in cat and rabbit CVM independent of the Mg2+i concentration ([Mg2+]i) at 37 degrees, 15 degrees, 10 degrees, and 5 degrees C. Reduced [Mg2+]i at low temperature (15 degrees C), shifted the voltage dependence of guinea pig IK1 activation in the depolarizing direction; this resulted in an apparent linearization of IK1 conductance. When the range of the membrane potential examined was expanded to include voltages up to +80 mV, the guinea pig IK1 was found to exhibit inward rectification with the inflection in the I-V relationship that is found at approximately EK at normal temperature, also shifted 80 mV or more to much less negative voltages at low temperatures. In contrast, irrespective of [Mg2+]i or temperature, the voltage dependencies of the IK1 activation curves for both cat and rabbit myocytes were not changed from that defined when [Mg2+]i was 1 mM and temperature was 37 degrees C. We propose that Mg2+i affects inward rectification of IK1 in cold guinea pig CVM by altering the voltage dependence of activation.
authors.affiliation: Department of Molecular Pharmacology and Biological Chemistry, Northwestern University, Chicago, IL 60611, USA.
authors.forename: R L
authors.initials: RL
authors.lastname: Martin
authors.forename: S
authors.initials: S
authors.lastname: Koumi
authors.forename: R E
authors.initials: RE
authors.lastname: Ten Eick
mesh_terms: D000818:Animals; D002415:Cats; D002478:Cells, Cultured; D004533:Egtazic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D004553:Electric Conductivity; D006168:Guinea Pigs; D006321:Heart / Q000187:drug effects / Q000502:physiology*; D006352:Heart Ventricles; D007202:Indicators and Reagents; D008274:Magnesium / Q000378:metabolism* / Q000494:pharmacology*; D018408:Patch-Clamp Techniques; D015221:Potassium Channels / Q000502:physiology*; D024661:Potassium Channels, Inwardly Rectifying; D011817:Rabbits; D013045:Species Specificity; D013696:Temperature
chemical_list: D007202:Indicators and Reagents; D015221:Potassium Channels; D024661:Potassium Channels, Inwardly Rectifying; D004533:Egtazic Acid; D008274:Magnesium; C025603:1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid