Aims: We investigated the role of the inward rectifier K(+) channel (K(IR)) in the renal interlobular artery (ILA). The ILA supplies the afferent arteriole and ranges in diameter from >100 µm near its origin at the arcuate artery to <30 µm at its most distal segment.
Methods and results: Vasodilatory responses to elevated extracellular K(+) (15 mmol/L) and vasoconstrictor responses due to K(IR) blockade by Ba(2+) (10-100 µmol/L) were assessed in in vitro perfused hydronephrotic rat kidneys. The distal ILA (26 ± 1 µm) exhibited K(+)-induced dilation and Ba(2+)-induced vasoconstriction, whereas neither response was observed in the proximal ILA (108 ± 3 µm). The intermediate ILA (55 ± 1 µm) exhibited a modest K(+)-induced vasodilatation, but no Ba(2+)-induced vasoconstriction. The K(+)-induced dilations were blocked by Ba(2+), but not by ouabain. Ba(2+)-induced depolarization, measured in ILA segments from normal kidneys, decreased with the increasing diameter. Patch-clamp studies demonstrated that the K(IR) current (I(KIR)) density also was inversely correlated with ILA segment diameter. Myocytes from afferent arterioles and distal ILAs exhibited similarly large I(KIR), whereas this current was absent in proximal ILA myocytes. Finally, we found that Ba(2+) attenuated myogenic vasoconstriction, suggesting an involvement of I(KIR). The previously shown pattern of myogenic reactivity of the ILA (distal > intermediate > proximal) mirrors the distribution of I(KIR) reported in the present study, further supporting a role for I(KIR).
Conclusion: Our findings indicate differences in the magnitude of I(KIR) along the ILA and suggest that the influence of K(IR) on reactivity increases as vessel diameter decreases from proximal to distal regions.