From the Department of Physiology, Tulane University School of Medicine,
New Orleans, La.
Correspondence to Atsuhiro Ichihara, MD, PhD, Department of Physiology, Tulane University School of Medicine, 1430 Tulane Ave, New Orleans, LA 70112. E-mail ichihara{at}mailhost.tcs.tulane.edu
Abstract—The present study was
conducted to determine the contribution of nitric oxide to
angiotensin II (Ang II) reactivity of afferent and efferent
arterioles from Ang II–infused hypertensive rats. Experiments were
performed in vitro with the blood-perfused juxtamedullary nephron
technique in kidneys harvested from hypertensive Sprague-Dawley rats
(181±1 mm Hg) that had received 60 ng/min Ang II subcutaneously
for 13 days. Superfusion with 0.1, 1, and 10 nmol/L Ang II reduced
afferent arteriolar diameter (18.1±0.6 µm; n=12) by
10.0±0.7%, 28.1±1.7%, and 52.8±1.9%, respectively, and efferent
arteriolar diameter (17.2±1.4 µm; n=8) decreased by 9.3±0.7%,
27.0±1.2%, and 50.4±1.6%, respectively. Nitric oxide synthase
inhibition with 100 µmol/L
N
© 1998 American Heart Association, Inc.
Scientific Contributions
Interactive Nitric Oxide–Angiotensin II Influences on Renal Microcirculation in Angiotensin II–Induced Hypertension
-nitro-L-arginine (NLA)
reduced resting afferent and efferent arteriolar diameters to 14.7±0.4
and 14.3±1.2 µm, respectively, and enhanced afferent but not
efferent arteriolar reactivity to Ang II. The enhanced afferent
arteriolar reactivity to Ang II was eliminated by addition of the
nitric oxide donor
S-nitroso-N-acetylpenicillamine (SNAP,
10 µmol/L), which reversed the NLA-induced decrease in diameter.
Addition of 10 µmol/L SNAP, without NLA, blunted efferent but
not afferent arteriolar reactivity to Ang II. Afferent (n=7) and
efferent arteriolar diameters (n=6) decreased by 48.5±2.2% and
41.0±1.9%, respectively, in response to 10 nmol/L Ang II. These
results suggest that in this model of hypertension, maintained nitric
oxide production in afferent arterioles counteracts the
enhanced afferent arteriolar reactivity that occurs in Ang
II–induced hypertension.
Key Words: rats • kidney • arterioles • nitric oxide • angiotensin II
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