期刊
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
卷 281, 期 3, 页码 C1029-C1037出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpcell.2001.281.3.C1029
关键词
cerebral arteries; smooth muscle; ryanodine receptors; cAMP-dependent protein kinase; ion channels; calcium; potassium; adenosine 3 ',5 '-cyclic monophosphate
资金
- NHLBI NIH HHS [F32-HL-09920, HL44455, HL63722] Funding Source: Medline
- NINDS NIH HHS [NS-39405] Funding Source: Medline
- OCPHP CDC HHS [P40 PR-12358] Funding Source: Medline
Phospholamban (PLB) inhibits the sarcoplasmic reticulum. (SR) Ca2+-ATPase, and this inhibition is relieved by cAMP-dependent protein kinase (PKA)-mediated phosphorylation. The role of PLB in regulating Call release through ryanodine-sensitive Ca2+ release channels, measured as Ca2+ sparks, was examined using smooth muscle cells of cerebral arteries from PLB-deficient (knockout) mice (PLB-KO). Ca2+ sparks were monitored optically using the fluorescent Ca2+ indicator fluo 3 or electrically by measuring transient large-conductance Ca2+-activated K+ (BK) channel currents activated by Call sparks. Basal Ca2+ spark and transient BK current frequency were elevated in cerebral artery myocytes of PLB-KO mice. Forskolin, an activator of adenylyl cyclase, increased the frequency of Ca2+ sparks and transient BK currents in cerebral arteries from control mice. However, forskolin had little effect on the frequency of Call sparks and transient BK currents from PLB-KO cerebral arteries. Forskolin or PLB-KO increased SR Ca2+ load, as measured by caffeine-induced Ca2+ transients. This study provides the first evidence that PLB is critical for frequency modulation of Ca2+ sparks and associated BK currents by PKA in smooth muscle.
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