Abstract
Large conductance Ca2+‐activated potassium channels (BKCa) channels are targeted to caveolae microdomains, where Cav‐1 interacts with BK(Ca) channels. The functional consequence of this interaction and its impact on EDHF‐mediated arteriolar dilation is not known. Thus, in this study we set out to examine the role of Cav‐1 in modulating the contribution of BK(Ca) channels to EDHF‐mediated arteriolar dilations. In isolated, pressurized (80 mmHg) gracilis muscle arterioles (≈ 100 μm) of Cav‐1 knockout mice, ACh‐induced, EDHF‐mediated dilations were enhanced (88±5 vs. 79±4 %) and were significantly reduced by selective BK(Ca) channel inhibitor, iberiotoxin (IBTX) (50±6 %), while IBTX had no effect on EDHF‐mediated dilations in wild type mice (75±7 %). Dilations to selective BK(Ca) opener, NS‐1619 were augmented in Cav‐1 knockout mice (58±6 % vs. 26±3 %). Moreover, in control arterioles, disruption of caveolae with methyl‐ß‐cyclodextrin augmented IBTX sensitive, ACh‐induced (29±7 % dilation in the presence of IBTX), and also NS‐1619‐evoked dilations (55±10 %). Immunohistochemistry demonstrated a co‐localization of Cav‐1 and BK(Ca) channels in the smooth muscle layer of control arterioles. Thus, we concluded that under control conditions an interaction between Cav‐1 and BK(Ca) channel limits the contribution of BK(Ca) channel to EDHF‐mediated arteriolar dilation. (AHA 0735540T)
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