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Ca2+ and Sr2+ entry induced Ca2+ release from the intracellular Ca2+ store in smooth muscle cells of rat portal vein.
Author(s) -
Grégoire G,
Loirand G,
Pacaud P
Publication year - 1993
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1993.sp019957
Subject(s) - depolarization , repolarization , biophysics , ryanodine receptor , membrane potential , chemistry , intracellular , caffeine , electrophysiology , medicine , biology , biochemistry
1. Changes in cytosolic free Ca2+ concentration ([Ca2+]i) induced by membrane depolarizations were investigated using indo‐1 microspectrofluorimetry in single patch‐clamped smooth muscle cells of rat portal vein at room temperature (20‐21 degrees C) and in the presence of 2 mM Ca2+. 2. During a 1 s depolarization from ‐50 to ‐30 mV [Ca2+]i rose, but, although the Ca2+ current was terminated by repolarization to ‐50 mV, [Ca2+]i continued to increase in a regenerative manner. The delay between the end of the voltage step and the peak of the [Ca2+]i rise was reduced by increasing the depolarization. 3. When a second identical depolarization was rapidly applied (8‐13s) after the first one, it induced an identical Ca2+ current but a smaller increase in [Ca2+]i which started to decay upon repolarization. 4. A low concentration of caffeine (0.05 mM), applied to cells showing a small depolarization‐induced [Ca2+]i transient which reached a peak at the end of the voltage step, produced an increase in amplitude and in duration of the [Ca2+]i rise without changing the amplitude of the depolarization‐induced Ca2+ current. 5. The depolarization‐induced [Ca2+]i rise was shortened and reduced in amplitude after noradrenaline‐ (NA 10 microM) or caffeine‐ (5 mM) induced release of Ca2+ store and when the patch pipette solution contained ryanodine (100 microM). Under these conditions, the depolarization‐induced [Ca2+]i transient was maximal at the end of the voltage step and declined immediately when the membrane was repolarized at ‐50 mV. 6. Experiments were done by replacing extracellular Ca2+ by Sr2+. Depolarization‐induced Sr2+ entry through voltage‐dependent Ca2+ channels could evoke an increase in indo‐1 fluorescence which occurred after the termination of the voltage step. This delayed component of fluorescence increase displayed properties similar to those of the regenerative [Ca2+]i rise recorded in the Ca(2+)‐containing solution. 7. The inefficiency of the second of two successive depolarizations to produce the delayed component of [Ca2+]i rise was not due to the emptiness of the intracellular Ca2+ store since, under these conditions, caffeine was still able to induce a Ca2+ release. 8. It is concluded that depolarization‐evoked Ca2+ or Sr2+ entry through voltage‐dependent Ca2+ channels induced the release of Ca2+ from an intracellular store, which could occur in a regenerative manner, independent of the termination of the triggering current.