Key Points
- To determine the effects of nitric oxide synthase inhibition on basal tone and agonist-induced vasodilation in isolated renal afferent and efferent arterioles.
- Afferent and efferent arterioles isolated from rabbit kidneys were treated with nitric oxide synthase inhibitors, N omega-nitro-L-arginine (10⁻⁷ to 10⁻³ M) and NG-monomethyl-L-arginine (3 x 10⁻⁴ M), under basal conditions.
- Vascular responses to endothelium-dependent (acetylcholine) and endothelium-independent (prostaglandin E2, dopamine) vasodilators were measured in norepinephrine-precontracted arterioles, with stereospecific reversal tested using L- and D-arginine.
- Under basal conditions, N omega-nitro-L-arginine caused a 40% decrease in the lumen diameter of afferent arterioles but had no effect on efferent arteriole diameter.
- Both nitric oxide synthase inhibitors markedly attenuated acetylcholine-induced vasorelaxation in precontracted afferent and efferent arterioles, an effect reversed by 10⁻³ M L-arginine but not D-arginine.
- Inhibition of nitric oxide synthase did not alter vasodilation elicited by prostaglandin E2 in afferent arterioles or dopamine in efferent arterioles.
Structured PICO
PPopulationAfferent and efferent arterioles isolated from rabbit kidneys
IInterventionNitric oxide synthase inhibitors (N omega-nitro-L-arginine [10(-7) to 10(-3) M] and NG-monomethyl-L-arginine [3 x 10(-4) M])
CComparatorBasal conditions; reversal with L-arginine vs D-arginine; endothelium-independent vasodilators (prostaglandin E2 and dopamine)
OOutcomeArteriole lumen diameter and vasorelaxant response to acetylcholinesurrogate
This in vitro study demonstrates that afferent, but not efferent, renal arterioles synthesize and release nitric oxide in the basal state, highlighting its role in regulating renal hemodynamics.