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Cardiovascular-Renal Mechanisms in Health and Disease

Superoxide mediates acute renal vasoconstriction produced by angiotensin II and catecholamines by a mechanism independent of nitric oxide

¹Department of Cell and Molecular Physiology; ²Carolina Cardiovascular Biology Center; and ³UNC Kidney Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina

Submitted 5 July 2006 ; accepted in final form 28 August 2006

NAD(P)H oxidases (NOX) and reactive oxygen species (ROS) are involved in vasoconstriction and vascular remodeling during hypertension produced by chronic angiotensin II (ANG II) infusion. These effects are thought to be mediated largely through superoxide anion (O₂^–) scavenging of nitric oxide (NO). Little is known about the role of ROS in acute vasoconstrictor responses to agonists. We investigated renal blood flow (RBF) reactivity to ANG II (4 ng), norepinephrine (NE, 20 ng), and ₁-adrenergic agonist phenylephrine (PE, 200 ng) injected into the renal artery (ira) of anesthetized Sprague-Dawley rats. The NOX inhibitor apocynin (1–4 mg·kg^–1·min^–1 ira, 2 min) or the superoxide dismutase mimetic Tempol (1.5–5 mg·kg^–1·min^–1 ira, 2 min) rapidly increased resting RBF by 8 ± 1% (P < 0.001) or 3 ± 1% (P < 0.05), respectively. During NO synthase (NOS) inhibition (N-nitro-L-arginine methyl ester, 25 mg/kg iv), the vasodilation tended to increase (apocynin 13 ± 4%, Tempol 10 ± 1%). During control conditions, both ANG II and NE reduced RBF by 24 ± 4%. Apocynin dose dependently reduced the constriction by up to 44% (P < 0.05). Similarly, Tempol blocked the acute actions of ANG II and NE by up to 48–49% (P < 0.05). In other animals, apocynin (4 mg·kg^–1·min^–1 ira) attenuated vasoconstriction to ANG II, NE, and PE by 46–62% (P < 0.01). During NOS inhibition, apocynin reduced the reactivity to ANG II and NE by 60–72% (P < 0.01), and Tempol reduced it by 58–66% (P < 0.001). We conclude that NOX-derived ROS substantially contribute to basal RBF as well as to signaling of acute renal vasoconstrictor responses to ANG II, NE, and PE in normal rats. These effects are due to O₂^– rather than H₂O₂, occur rapidly, and are independent of scavenging of NO.

hemodynamics; vascular smooth muscle; renal vascular resistance; afferent arteriole; oxidative stress; reactive oxygen species; redox signaling

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