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1 Department of Physiology, University of Tennessee Health Science Center, Memphis, Tennessee, United States
* To whom correspondence should be addressed. E-mail: jjaggar{at}physio1.utmem.edu.
In smooth muscle cells, localized intracellular calcium (Ca2+) transients, termed "Ca2+ sparks", activate several large-conductance Ca2+-activated potassium (KCa) channels, resulting in a transient KCa current. In some smooth muscle cell types, a significant proportion of Ca2+ sparks do not activate KCachannels. The goal of this study was to explore mechanisms that underlie fractional Ca2+ spark to KCa channel coupling. We investigated if membrane depolarization or ryanodine-sensitive Ca2+ release (RyR) channel activation modulates coupling in newborn (1-3 day old) porcine cerebral artery myocytes. At steady membrane potentials of -40, 0 and +40 mV, mean transient KCa current frequency was ~0.18, 0.43, and 0.26 Hz and KCa channel activity (NPO) at the transient KCa current peak was ~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 ~1.6-fold. In contrast, caffeine (10µM), a RyR channel activator, increased mean transient KCa current frequency, but did not alter Ca2+ spark to 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 causing fractional Ca2+ spark uncoupling in newborn cerebral artery myocytes.
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