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(Circulation Research. 1996;78:717-723.)
© 1996 American Heart Association, Inc.

Articles

Effect of Membrane Potential on the Initiation of Acetylcholine-Induced Ca²⁺ Transients in Isolated Guinea Pig Coronary Myocytes

Vladimir Y. Ganitkevich, Gerrit Isenberg

From the Department of Physiology (V.Y.G.), University of Cologne (Germany) and the Department of Physiology (G.I.), University of Halle (Germany).

Correspondence to Dr V.Y. Ganitkevich, Department of Physiology, University of Cologne, Robert-Koch-Str. 39, 50931 Köln, Germany.

Abstract The muscarinic stimulation of single voltage-clamped coronary arterial smooth muscle cells of the guinea pig was used to evaluate the effect of membrane potential on the inositol 1,4,5-tris-phosphate (IP₃)–mediated changes of ionized [Ca²⁺] in the cytoplasm (Ca²⁺ transient) measured with indo 1. When applied at the membrane potential of -50 mV, 10 µmol/L acetylcholine (ACh) induced a [Ca²⁺]_i increase after the mean latency of 2.6±0.9 s. The latency was reduced to 1.1±0.3 s when the same dose was applied at a holding potential of +50 mV. In paired experiments in the same cells, the latency of response at +50 mV was reduced by a factor of 2.2±0.3 compared with the response at -50 mV. Supramaximal [ACh] (100 µmol/L) induced Ca²⁺ transients with a 0.4±0.1-s latency, which was independent of membrane potential. When applied repetitively at -50 mV, ACh induced Ca²⁺ transients with a progressively reduced amplitude and slower rate of rise. Depolarization to +50 mV accelerated the rate of rise of the Ca²⁺ transient by a factor of 3.4±0.4 without affecting the amplitude. The modulation of the initiation of Ca²⁺ transient by a 100-mV depolarization can be explained by an approximately threefold increase in the rate of IP₃ accumulation.

Key Words: acetylcholine • membrane potential • Ca²⁺ transients

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