BK Ca and K V channels modify remote Ca 2+ responses to local depolarization in rat mesenteric arterioles

Conducted vasoconstriction plays an important role in determining microvascular resistance. The spread of depolarization along an arteriole occurs through cell‐cell coupling via gap junctions. The decay of conducted depolarization is characterized by the length constant λ, and depends on the membrane (r m ) and junctional resistances (r j ) as follows: λ=v(r m /r j ). We hypothesized that this decay can be diminished by increasing r m through inhibition of K + channels. We investigated this hypothesis in rat mesenteric terminal arterioles (<40 µm) by monitoring local and remote Ca 2+ responses to localized delivery of 155 mM KCl. Ca 2+ responses were recorded simultaneously at 6 positions along a short arteriolar segment and λ was estimated by non‐linear curve‐fitting. The K V channel blocker 4‐AP (1 mM) augmented the remote Ca 2+ responses (λ increased from 296 ± 30 to 417 ± 64 µm; P=0.05, n=5). The BK Ca channel blocker IbTx (100 nM) increased λ from 254 ± 37 to 343 ± 54 µm (P<0.01, n=6). Preconstriction of arterioles (norepinephrine + neuropeptide Y) increased λ from 289 ± 37 to 336 ± 40 µm (P<0.05; n=6), and subsequent addition of IbTx further increased λ to 425 ± 59 µm (P<0.01; n=6). BK Ca , K V 1.5, and K V 2.1 channels were immuno‐localized to VSMC. These data are consistent with the idea that BK Ca and K V channel expression modulates conduction of depolarization through an effect on smooth muscle r m in mesenteric arterioles.