Premium
Oxidative stress contributes to altered K+ channel regulation of afferent arteriolar tone in diabetic rat kidney
Author(s) -
Troncoso Brindeiro Carmen M,
Fallet Rachel W,
Carmines Pamela K
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.667.13
Rats with streptozotocin (STZ)‐induced diabetes exhibit an increased tonic dilator impact of ATP‐sensitive K+ channels (KATP) and other inward‐rectifier K+ (Kir) channels on renal afferent arterioles. We hypothesized that oxidative stress underlies this phenomenon. Nondiabetic (Sham) and STZ rats were left untreated or received tempol (6–11 μmol/day) for 3 wk. The in vitro blood‐perfused juxtamedullary nephron technique was used to quantify afferent arteriolar lumen diameter responses to the Kir channel blockers Ba2+ (10–100 μM), tertiapin‐Q (TPQ, 1–100 nM), and glibenclamide (GB, 30–300 μM). The decrease in lumen diameter evoked by 100 μM Ba2+ was greater in STZ rats (35±6%) than in sham rats (11±3%, P<0.05). In STZ rats, 300 μM GB decreased afferent diameter by 21±11% and 100 nM TPQ decreased diameter by 11±3% (both P<0.05 vs baseline), but these treatments had no effect on arterioles from Sham rats. Exaggerated contractile responses to Ba2+, TPQ, and GB were not evident in kidneys from tempol‐treated STZ rats. K+ channel mRNA expression and protein levels in preglomerular microvessels did not differ between Sham and STZ and were unaffected by tempol. DHE staining was increased in cortical microvessels and tubules of STZ kidneys compared to sham; this effect was abolished by tempol. Our data suggest that oxidative stress contributes to the exaggerated impact of Kir channels on afferent arteriolar tone in STZ rats.