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Impaired flow‐induced dilation in coronary arterioles of dogs fed a low‐salt diet
Author(s) -
Sun Dong,
Yan Changdong,
Cheng Jennifer,
Jacobson Azita,
Huang An,
Kaley Gabor,
Hintze Thomas H
Publication year - 2007
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.21.5.a449-c
Subject(s) - apocynin , nadph oxidase , superoxide , medicine , chemistry , angiotensin ii , coronary arteries , endocrinology , vasodilation , arteriole , endothelial dysfunction , nitric oxide , artery , microcirculation , oxidative stress , biochemistry , blood pressure , enzyme
Low‐salt diet is considered to be helpful in prevention and treatment of hypertension. However, sodium restriction increases the production of angiotensin II and may induce counter‐regulatory responses. To this end, we examined the effect of low‐salt diet on superoxide formation and endothelial function in coronary arterioles. Dogs were fed with a low‐salt diet (0.5% NaCl) for 2–3 weeks. Compared with normal dogs, plasma angiotensin II increased 3 fold and flow‐induced dilation (FID) of coronary arterioles decreased by 60% in low‐salt fed dogs. In normal dogs, FID of coronary arterioles is mainly a NO‐mediated response. However, in low‐salt fed dogs, the inhibition of NO synthesis (L‐NAME; 300 μM) had no significant effect on FID but administration of apocynin (10 μM), a selective inhibitor of NADPH oxidase, which had no effect on FID in normal dogs, significantly enhanced FID. Western blot analysis revealed a two‐fold increase in gp91phox in coronary arteries of low‐salt fed dogs. Superoxide formation in the endothelial and smooth muscle layers of coronary arteries was assessed by dihydroethidium staining and confocal microscopy. In cannulated, pressurized coronary arteries, administration of apocynin resulted in a greater reduction of superoxide formation in dogs fed a low‐salt diet. We conclude that long‐term low‐salt diet impairs endothelial function of coronary arterioles by decreasing NO bioavailability via an increased angiotensin‐NADPH oxidase‐dependent superoxide formation. (NIH HL‐68813, HL‐43023 and HL‐083647)