title: Caffeine- and histamine-induced oscillations of K(Ca) current in single smooth muscle cells of rabbit cerebral artery.
abstract: In the present experiment, we characterized the intracellular Ca2+ oscillations induced by caffeine (1mM) or histamine (1-3microM) in voltage-clamped single smooth muscle cells of rabbit cerebral (basilar) artery. Superfusion of caffeine or histamine induced periodic oscillations of large whole-cell K+ current with fairly uniform amplitudes and intervals. The oscillatory K+ current was abolished by inclusion of ethylenebis(oxonitrilo)tetraacetate (EGTA, 5mM) in the pipette solution. Caffeine- and histamine-induced periodic activation of the large-conductance Ca2+-activated K+ [K(Ca)] channel was recorded in the cell-attached patch mode. These results suggest that the oscillations of K+ current are carried by the K(Ca) channel and reflect the oscillations of intracellular Ca2+ concentration ([Ca2+]i). Ryanodine (1-10microM) abolished both caffeine- and histamine-induced oscillations. Caffeine-induced oscillations were abolished by the sarcoplasmic reticulum Ca2+-adenosine 5'-triphosphatase (Ca2+-ATPase) inhibitor, cyclopiazonic acid (10microM), and a high concentration of caffeine (10mM). Inclusion of heparin (3mg/ml) in the pipette solution blocked histamine-induced oscillations, but did not block caffeine-induced oscillations. By the removal of extracellular Ca2+, but not by the addition of verapamil and Cd2+, the caffeine-induced oscillations were abolished. Increasing Ca2+ influx rate increased the frequencies of caffeine-induced oscillations. Spontaneous oscillations were also observed in cells that were not superfused with agonists, and had similar characteristics to the caffeine-induced oscillations. From the above results, it is concluded, that in smooth muscle cells of the rabbit cerebral (basilar) artery, ryanodine-sensitive Ca2+-induced Ca2+ release pools play key roles in the generation of caffeine- and histamine-induced intracellular Ca2+ oscillations.
authors.affiliation: Department of Physiology and Biophysics, Seoul National University College of Medicine, 28 Yongon-Dong, Chongno-Gu, Seoul 110-799, Korea.
authors.forename: T M
authors.initials: TM
authors.lastname: Kang
authors.forename: I
authors.initials: I
authors.lastname: So
authors.forename: K W
authors.initials: KW
authors.lastname: Kim
mesh_terms: D000818:Animals; D001488:Basilar Artery / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D002110:Caffeine / Q000494:pharmacology*; D002118:Calcium / Q000502:physiology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D000252:Calcium-Transporting ATPases / Q000037:antagonists & inhibitors; D004594:Electrophysiology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006632:Histamine / Q000494:pharmacology*; D066298:In Vitro Techniques; D007211:Indoles / Q000494:pharmacology; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D018408:Patch-Clamp Techniques; D015221:Potassium Channels / Q000187:drug effects / Q000378:metabolism*; D011817:Rabbits
chemical_list: D002121:Calcium Channel Blockers; D004791:Enzyme Inhibitors; D007211:Indoles; D015221:Potassium Channels; D002110:Caffeine; D006632:Histamine; D000252:Calcium-Transporting ATPases; D002118:Calcium; C000543:cyclopiazonic acid