Segment-specific differences in the inward rectifier K+ current along the renal interlobular artery

Journal Publication ResearchOnline@JCU
Chilton, Lisa;Smirnov, Sergey V.;Loutzenhiser , Kathy;Wang, Xuemei;Loutzenhiser, Rodger
Abstract

Aims: We investigated the role of the inward rectifier K+ channel (KIR) 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 KIR blockade by Ba2+ (10–100 µmol/L) were assessed in in vitro perfused hydronephrotic rat kidneys. The distal ILA (26 ± 1 µm) exhibited K+-induced dilation and Ba2+-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 Ba2+-induced vasoconstriction. The K+-induced dilations were blocked by Ba2+, but not by ouabain. Ba2+-induced depolarization, measured in ILA segments from normal kidneys, decreased with the increasing diameter. Patch-clamp studies demonstrated that the KIR current (IKIR) density also was inversely correlated with ILA segment diameter. Myocytes from afferent arterioles and distal ILAs exhibited similarly large IKIR, whereas this current was absent in proximal ILA myocytes. Finally, we found that Ba2+ attenuated myogenic vasoconstriction, suggesting an involvement of IKIR. The previously shown pattern of myogenic reactivity of the ILA (distal > intermediate > proximal) mirrors the distribution of IKIR reported in the present study, further supporting a role for IKIR. Conclusion: Our findings indicate differences in the magnitude of IKIR along the ILA and suggest that the influence of KIR on reactivity increases as vessel diameter decreases from proximal to distal regions.

Journal

Cardiovascular research

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Volume

92

ISBN/ISSN

1755-3245

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Issue

1

Pages Count

9

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Publisher

Elsevier

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N/A

DOI

10.1093/cvr/cvr179