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Ca 2+ ‐activated K + channels are controlled by Ca 2+ influx through voltage‐gated Ca 2+ channels, not the release of Ca 2+ through ryanodine receptors in arteriolar smooth muscle
Author(s) -
Boerman Erika Mary,
Jackson William F.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1142.2
Subject(s) - chemistry , tetraethylammonium , ryanodine receptor , biophysics , endoplasmic reticulum , potassium , biochemistry , biology , organic chemistry
Ca 2+ from ryanodine receptors (RYR) does not control the activity of Ca 2+ ‐activated K + channels (BK Ca ) in microvascular smooth muscle (μVSM), unlike other systems. To further test this hypothesis, hamster cremaster arterioles were isolated, cannulated, pressurized to 80 cm H 2 O, loaded with Fluo 4 and confocally imaged. In vessels with myogenic tone under control conditions, we saw no Ca 2+ sparks, but Ca 2+ flashes were seen in 39% of μVSM (n = 198). Phenylephrine (1 μM) increased sparks (9%) and flashes (88%) (n = 207, p < 0.05). To test if Ca 2+ entry through voltage‐gated Ca 2+ channels (VGCC) controls BK Ca , we measured diameter responses at 20 cm H 2 O to the BK Ca antagonist, tetraethylammonium (TEA, 1 mM) in the absence and presence of a VGCC agonist, BayK 8644 (~5 nM). TEA alone caused only a 2 ± 1 μm constriction. BayK constricted vessels from 50 ± 2 μm to 38 ± 2 μm (p < 0.05). With BayK, TEA constrictions increased to 16 ± 1 μm (n = 8, p < 0.05). In Fluo 4 loaded vessels at 20 cm H 2 O, no Ca 2+ sparks were observed, and flashes were seen in only 25% of μVSM (n = 163). In the presence of BayK, a few sparks were observed (3%), but flashes increased substantially to 87% (n = 177, p < 0.05) along with a 55% increase in global Fluo 4 intensity. Our data indicate that the activity of BK Ca are not coupled to RYR in μVSM. Instead, our findings support the hypothesis that Ca 2+ entry through VGCC controls BK Ca activity in arterioles. Supported by PHS grant HL32469 to WFJ.