Potassium channel contributions to afferent arteriolar tone in normal and diabetic rat kidney

We previously reported an enhanced tonic dilator impact of ATP- sensitive K+ channels in afferent arterioles of rats with streptozotocin (STZ)induced diabetes. The present study explored the hypothesis that other types of K+ channel also contribute to afferent arteriolar dilation in STZ rats. The in vitro blood-perfused juxtamedullary nephron technique was utilized to quantify afferent arteriolar lumen diameter responses to K+ channel blockers: 0.1-3.0 mM 4-aminopyridine (4-AP; KV channels), 10-100 mu M barium (K-IR channels), 1-100 nM tertiapin-Q (TPQ; Kir1.1 and Kir3. x subfamilies of K-IR channels), 100 nM apamin (SKCa channels), and 1 mM tetraethylammonium (TEA; BKCa channels). In kidneys from normal rats, 4-AP, TEA, and Ba2+ reduced afferent diameter by 23 +/- 3, 8 +/- 4, and 18 +/- 2%, respectively, at the highest concentrations employed. Neither TPQ nor apamin significantly altered afferent diameter. In arterioles from STZ rats, a constrictor response to TPQ (22 +/- 4% decrease in diameter) emerged, and the response to Ba2+ was exaggerated (28 +/- 5% decrease in diameter). Responses to the other K+ channel blockers were similar to those observed in normal rats. Moreover, exposure to either TPQ or Ba2+ reversed the afferent arteriolar dilation characteristic of STZ rats. Acute surgical papillectomy did not alter the response to TPQ in arterioles from normal or STZ rats. We conclude that 1) K-V, K-IR, and BKCa channels tonically influence normal afferent arteriolar tone, 2) K-IR channels (including Kir1.1 and/ or Kir3. x) contribute to the afferent arteriolar dilation during diabetes, and 3) the dilator impact of Kir1.1/ Kir3. x channels during diabetes is independent of solute delivery to the macula densa.