Aim: We tested the hypothesis that K_V7 channels contribute to basal renal vascular tone and that they participate in agonist-induced renal vasoconstriction or vasodilation.
Methods: K_V7 channel subtypes in renal arterioles were characterized by immunofluorescence. Renal blood flow (RBF) was measured using an ultrasonic flow probe. The isometric tension of rat interlobar arteries was examined in a wire myograph. Mice afferent arteriolar diameter was assessed utilizing the perfused juxtamedullary nephron technique.
Results: Immunofluorescence revealed that K_V7.4 channels were expressed in rat afferent arterioles. The K_V7 blocker XE991 dose-dependently increased the isometric tension of rat interlobar arteries and caused a small (approx. 4.5%) RBF reduction in vivo. Nifedipine abolished these effects. Likewise, XE991 reduced mouse afferent arteriolar diameter by approx. 5%. The K_V7.2–5 stimulator flupirtine dose-dependently relaxed isolated rat interlobar arteries and increased (approx. 5%) RBF in vivo. The RBF responses to NE or Ang II administration were not affected by pre-treatment with XE991 or flupirtine. XE991 pre-treatment caused a minor augmentation of the acetylcholine-induced increase in RBF, while flupirtine pre-treatment did not affect this response.
Conclusion: It is concluded that K_V7 channels, via nifedipine sensitive channels, have a role in the regulation of basal renal vascular tone. There is no indication that K_V7 channels have an effect on agonist-induced renal vasoconstriction while there is a small effect on acetylcholine-induced vasodilation.