Document Detail


KCa channel insensitivity to Ca2+ sparks underlies fractional uncoupling in newborn cerebral artery smooth muscle cells.
MedLine Citation:
PMID:  16603686     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
In smooth muscle cells, localized intracellular Ca2+ transients, termed "Ca2+ sparks," activate several large-conductance Ca2+-activated K+ (KCa) channels, resulting in a transient KCa current. In some smooth muscle cell types, a significant proportion of Ca2+ sparks do not activate KCa channels. The goal of this study was to explore mechanisms that underlie fractional Ca2+ spark-KCa channel coupling. We investigated whether membrane depolarization or ryanodine-sensitive Ca2+ release (RyR) channel activation modulates coupling in newborn (1- to 3-day-old) porcine cerebral artery myocytes. At steady membrane potentials of -40, 0, and +40 mV, mean transient KCa current frequency was approximately 0.18, 0.43, and 0.26 Hz and KCa channel activity [number of KCa channels activated by Ca2+ sparksxopen probability of KCa channels at peak of Ca2+ sparks (NPo)] at the transient KCa current peak was approximately 4, 12, and 24, respectively. Depolarization between -40 and +40 mV increased KCa channel sensitivity to Ca2+ sparks and elevated the percentage of Ca2+ sparks that activated a transient KCa current from 59 to 86%. In a Ca2+-free bath solution or in diltiazem, a voltage-dependent Ca2+ channel blocker, steady membrane depolarization between -40 and +40 mV increased transient KCa current frequency up to approximately 1.6-fold. In contrast, caffeine (10 microM), an RyR channel activator, increased mean transient KCa current frequency but did not alter Ca2+ spark-KCa channel coupling. These data indicate that coupling is increased by mechanisms that elevate KCa channel sensitivity to Ca2+ sparks, but not by RyR channel activation. Overall, KCa channel insensitivity to Ca2+ sparks is a prominent factor underlying fractional Ca2+ spark uncoupling in newborn cerebral artery myocytes.
Authors:
Anlong Li; Adebowale Adebiyi; Charles W Leffler; Jonathan H Jaggar
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2006-04-07
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  291     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2006 Sep 
Date Detail:
Created Date:  2006-08-10     Completed Date:  2006-09-26     Revised Date:  2014-09-22    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H1118-25     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Animals, Newborn
Caffeine / pharmacology
Calcium / pharmacology*
Calcium Channel Blockers / pharmacology
Cell Communication / drug effects*,  physiology
Cell Membrane / physiology
Cerebral Arteries / cytology,  drug effects,  physiology*
Diltiazem / pharmacology
Electrophysiology
Membrane Potentials / physiology
Muscle, Smooth, Vascular / cytology,  drug effects,  physiology*
Potassium Channels, Calcium-Activated / drug effects*,  physiology
Ryanodine Receptor Calcium Release Channel / physiology
Swine
Grant Support
ID/Acronym/Agency:
HL-34059/HL/NHLBI NIH HHS; HL-42851/HL/NHLBI NIH HHS; HL-67061/HL/NHLBI NIH HHS; HL-77678/HL/NHLBI NIH HHS; R01 HL034059/HL/NHLBI NIH HHS; R01 HL067061/HL/NHLBI NIH HHS; R01 HL077678/HL/NHLBI NIH HHS; R37 HL042851/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Calcium Channel Blockers; 0/Potassium Channels, Calcium-Activated; 0/Ryanodine Receptor Calcium Release Channel; 3G6A5W338E/Caffeine; EE92BBP03H/Diltiazem; SY7Q814VUP/Calcium
Comments/Corrections

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