Pflügers Archiv : European journal of physiology. vol:429 issue:6 pages:797-804
Ca2+ release from the sarcoplasmic reticulum was studied in voltage-clamped guinea-pig atrial myocytes. Cells were dialysed with a pipette solution containing the Ca2+ indicator 1- [2-amino-5-(6-carboxyindol-2-yl) phenoxy]-2-(2'-amino-5'-methylphenoxy) ethane-N,N,N',N'-tetraacetic acid] (Indo-1, 100 microM) and as main anion either chloride or the low-affinity Ca2+ buffer citrate. Intracellular Ca2+ transients (Cai transients) were elicited by depolarizations from a holding potential of -50 mV. In chloride-dialysed cells, Cai transients showed a bell-shaped dependence on the amplitude of the depolarizing pulse. In citrate-dialysed cells, membrane depolarizations were associated with a small rise in [Ca2+]i. These small changes in [Ca2+]i were either followed by a large Cai transient or failed to induce large changes in [Ca2+]i. The peak amplitude of the large Cai transient did not vary with the amplitude of the depolarizing pulse. These results demonstrate that in the presence of intracellular chloride, Ca2+ release in atrial cells is a graded process triggered by Ca2+ influx. Using citrate as the main intracellular anoin, Ca2+ release triggered by Ca2+ entry was no longer graded but occurred in a regenerative manner. The results are discussed in terms of two models in which citrate, affects the spatial distribution of [Ca2+]i or the loading state of the sarcoplasmic reticulum.