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High Salt Diet –Induced Afferent Arteriolar Autoregulatory Dysfunction is Improved by Acute Antioxidant Treatment
Author(s) -
Inscho Edward W.,
Pollock David M.,
Pollock Jennifer S.,
Cook Anthony K.
Publication year - 2010
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.24.1_supplement.1059.9
Subject(s) - afferent arterioles , chemistry , endocrinology , autoregulation , medicine , vasoconstriction , perfusion , microcirculation , reactive oxygen species , blood pressure , oxidative stress , afferent , hemodynamics , vascular resistance , anatomy , biochemistry , angiotensin ii
High salt (HS) diet reduces myogenic reactivity in resistance arteries and autoregulatory responses of afferent arterioles. Oxidative stress is increased in HS rats. We tested the hypothesis that HS blunts autoregulatory behavior by stimulating accumulation of reactive oxygen species. Rats were fed a normal (NS, 0.4% NaCl) or HS (8% NaCl) diet for a period of 14 days. Baseline arteriolar diameter was similar between the NS and HS groups. Autoregulatory behavior was assessed by measuring diameter changes during step‐wise 15 mmHg increases in perfusion pressure from 65 to 170 mmHg. In NS kidneys, afferent arteriolar diameter decreased by 34 ± 2% (n=6) as perfusion pressure increased from 65 to 170 mmHg. In HS kidneys arteriolar diameter decreased by 6 ± 4% (P < 0.05; n = 8) indicating markedly attenuated pressure induced vasoconstriction. Acute exposure to Tempol (1.0 mM) in the superfusate had no effect on the autoregulatory response in NS rats but markedly improved autoregulation in the HS group. Increasing perfusion pressure from 65 to 170 mmHg in NS kidneys decreased afferent diameter by 32 ± 3% (n=3), whereas diameter decreased by 28 ± 3% (n=6) in kidneys from HS rats exposed to Tempol. These data indicate that reactive oxygen species blunt autoregulatory efficiency in kidneys from HS rats facilitating enhanced excretion of salt by buffering autoregulatory control of glomerular hemodynamics.