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Hyperpolarization and increased free calcium in acetylcholine-stimulated endothelial cells
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1988
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MechanobiologyMolecular PhysiologyTransient HyperpolarizationNeurophysiologyAtherosclerosisMedicinePhysiologyHyperpolarization (Biology)Endothelial DysfunctionCellular EventsVascular BiologySocial SciencesElectrophysiologyCardiovascular FunctionPharmacologyCellular PhysiologyFree CalciumSecondary Membrane Hyperpolarization
In freshly harvested aortic endothelial cells from rabbits, some cellular events associated with stimulation by acetylcholine (ACh) were analyzed. ACh (3 microM) induced a transient hyperpolarization of 8.3 +/- 2.5 mV, which peaked within 3-5 s and subsequently declined with a similar time course. Hyperpolarization was caused by a transient Ca2+-dependent outward current (IoACh), which was mainly carried by K+. ACh (3 and 10 microM) also evoked transient dose-dependent increases in the intracellular free Ca2+ concentration (Ca2+i). Pretreatment with atropine (1 and 3 microM) abolished both responses to ACh, the increase in Ca2+i as well as the transient outward current. It is concluded that IoACh and the rise in Ca2+i are two manifestations of muscarinic receptor stimulation. The rise in Ca2+i might be the primary event, leading to secondary membrane hyperpolarization.