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Tytuł:
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Ca2+ channels, ryanodine receptors and Ca(2+)-activated K+ channels: a functional unit for regulating arterial tone.
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Autorzy:
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Jaggar JH; Department of Pharmacology, University of Vermont, Burlington 05405, USA.
Wellman GC
Heppner TJ
Porter VA
Perez GJ
Gollasch M
Kleppisch T
Rubart M
Stevenson AS
Lederer WJ
Knot HJ
Bonev AD
Nelson MT
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Źródło:
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Acta physiologica Scandinavica [Acta Physiol Scand] 1998 Dec; Vol. 164 (4), pp. 577-87.
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Typ publikacji:
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Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.; Review
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Język:
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English
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Imprint Name(s):
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Publication: Oxford : Blackwell Scientific Publications
Original Publication: Stockholm.
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MeSH Terms:
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Calcium/*physiology
Calcium Channels/*physiology
Calcium Signaling/*physiology
Muscle, Smooth, Vascular/*physiology
Potassium Channels/*physiology
Ryanodine Receptor Calcium Release Channel/*physiology
Up-Regulation/*physiology
Animals ; Arteries/cytology ; Arteries/physiology ; Humans ; Muscle Tonus/physiology ; Muscle, Smooth, Vascular/cytology
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Liczba referencji:
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69
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Grant Information:
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GM14715 United States GM NIGMS NIH HHS; HL-44455 United States HL NHLBI NIH HHS; HL-51728 United States HL NHLBI NIH HHS
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Substance Nomenclature:
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0 (Calcium Channels)
0 (Potassium Channels)
0 (Ryanodine Receptor Calcium Release Channel)
SY7Q814VUP (Calcium)
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Entry Date(s):
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Date Created: 19990115 Date Completed: 19990407 Latest Revision: 20220311
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Update Code:
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20240104
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DOI:
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10.1046/j.1365-201X.1998.00462.x
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PMID:
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9887980
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Local calcium transients ('Ca2+ sparks') are thought to be elementary Ca2+ signals in heart, skeletal and smooth muscle cells. Ca2+ sparks result from the opening of a single, or the coordinated opening of many, tightly clustered ryanodine receptor (RyR) channels in the sarcoplasmic reticulum (SR). In arterial smooth muscle, Ca2+ sparks appear to be involved in opposing the tonic contraction of the blood vessel. Intravascular pressure causes a graded membrane potential depolarization to approximately -40 mV, an elevation of arterial wall [Ca2+]i and contraction ('myogenic tone') of arteries. Ca2+ sparks activate calcium-sensitive K+ (KCa) channels in the sarcolemmal membrane to cause membrane hyperpolarization, which opposes the pressure induced depolarization. Thus, inhibition of Ca2+ sparks by ryanodine, or of KCa channels by iberiotoxin, leads to membrane depolarization, activation of L-type voltage-gated Ca2+ channels, and vasoconstriction. Conversely, activation of Ca2+ sparks can lead to vasodilation through activation of KCa channels. Our recent work is aimed at studying the properties and roles of Ca2+ sparks in the regulation of arterial smooth muscle function. The modulation of Ca2+ spark frequency and amplitude by membrane potential, cyclic nucleotides and protein kinase C will be explored. The role of local Ca2+ entry through voltage-dependent Ca2+ channels in the regulation of Ca2+ spark properties will also be examined. Finally, using functional evidence from cardiac myocytes, and histological evidence from smooth muscle, we shall explore whether Ca2+ channels, RyR channels, and KCa channels function as a coupled unit, through Ca2+ and voltage, to regulate arterial smooth muscle membrane potential and vascular tone.
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