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KCNQ gene expression in the murine vasculature

KCNQ2‐5 are considered to be only expressed by neurones. Ohya et al. (Circ Res., 92, –1023, 2003) showed that full length KCNQ1 and a C‐terminal truncated variant were expressed in murine portal vein (mPV), where it contributed to vascular contractility. However, recent studies revealed that murine aorta and various conduit arteries expressed KCNQ4 and KCNQ5 abundantly. The present study used similar techniques that reinvestigated KCNQ channel gene expression in the mPV and analysed further the role of KCNQ expression products (Kv7.1‐5) in the vasculature. Nested PCR experiments revealed that KCNQ genes in addition to Q1 were present in the mPV and this was confirmed by immunocytochemical experiments with antibodies against KCNQ4 expression products. A functional role for ion channels encoded by KCNQ2‐5 was supported by electrophysiological and functional experiments with retigabine, an activator of ion channels encoded by all KCNQ genes except KCNQ1. Retigabine enhanced outward K+currents and relaxed spontaneous contractions of whole mPV. The KCNQ channel blocker XE991 contracted the aorta, carotid and femoral artery and the degree and rate of contraction was enhanced by contracting the tissue slightly with 0.1 μM phenylepherine. These data support a role for KCNQ channels in defining vascular reactivity.