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NADPH oxidase (NADPHox) contribution to Angiotensin II (AII)‐induced vasoconstriction is dependent on nitric oxide (NO) in normal rat conduction and resistance vessels
Author(s) -
SepúlvedaKattan Esteban,
Sepúlveda Patricia A,
Boric Mauricio P
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.21.6.a1229-b
Subject(s) - vasoconstriction , apocynin , vasodilation , angiotensin ii , contraction (grammar) , chemistry , medicine , endocrinology , phenylephrine , nadph oxidase , nitric oxide synthase , nitric oxide , biology , biochemistry , reactive oxygen species , blood pressure
AII induced vasoconstriction can be partially counteracted by inhibiting NADPHox and/or removing its product, superoxide anion (O 2 − ). Since NO, a potent endothelial‐derived vasodilator, is inactivated by O 2 − , we studied the contribution of NO sequestration by NADPHox activity in AII‐induced vasoconstriction in isolated conduit and resistance vessels. Aortic rings from normal male Sprague‐Dawley rats were mounted for recording isometric contraction at 2 g basal tension. Also, skeletal muscle arterioles (~200 μm diameter) were cannulated and perfused at 110 μL/min, 70 mmHg, to measure diameter by microscopy. Aired Tyrode‐HEPES buffer, pH 7.4, at 37°C was used. Responses to AII (10 −8 –10 −5 M aortic rings, 10 −5 M arterioles) and Phenylephrine (Phe 10 −5 M) were assessed in the absence and presence of NO synthase (NOS) inhibitor L‐NA 100μM, and/or NADPHox inhibitor Apocynin 100μM. In aortic rings, NOS inhibition increased responses to Phe and AII (~80–100%), whereas in arterioles, only Phe contraction was enhanced. In both preparations, Apocynin significantly reduced responses to AII (~20–30%), but did not affect Phe induced contraction. The attenuating effect of Apocynin on AII contraction was not observed in presence of LNA, indicating this effect was NO dependent. We conclude that NADPHox stimulation contributes to AII vasoconstriction mainly by NO inactivation in rat arteries and arterioles. Supported by Grant Fondecyt 1040816.