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(Hypertension. 1999;33:462-466.)
© 1999 American Heart Association, Inc.

Scientific Contributions

Neuronal Nitric Oxide Synthase-Dependent Afferent Arteriolar Function in Angiotensin II-Induced Hypertension

Atsuhiro Ichihara; John D. Imig; L. Gabriel Navar

From the Department of Physiology, Tulane University School of Medicine, New Orleans, La.

Correspondence to L. Gabriel Navar, PhD, Department of Physiology, Tulane University School of Medicine, 1430 Tulane Ave, New Orleans, LA 70112-2699. E-mail navar{at}mailhost.tcs.tulane.edu

Abstract—This study was designed to determine the influence of neuronal nitric oxide synthase (nNOS) in tubular flow-dependent regulation of afferent arteriolar diameter in hypertensive Sprague-Dawley rats that received 60 ng/min angiotensin II (Ang II) subcutaneously for 13 days. Systolic blood pressure of control and Ang II–infused rats averaged 122±2 (n=23) and 194±2 mm Hg (n=24). Afferent arteriolar responses to the nNOS inhibitor S-methyl-L-thiocitrulline (L-SMTC; 0.1 to 10 µmol/L) and the nonselective NOS inhibitor N-nitro-L-arginine (L-NNA; 1 to 100 µmol/L) were assessed in vitro using the blood-perfused juxtamedullary nephron preparation. At a perfusion pressure of 160 mm Hg, afferent arteriolar diameters from control and Ang II–infused rats averaged 18.7±1.1 µm (n=8) and 18.1±1.1 µm (n=9), respectively, and decreased by 19.9±1.5% and 11.8±1.1%, respectively, in response to 10 µmol/L L-SMTC. The L-SMTC–induced afferent arteriolar constriction was significantly greater in control than in Ang II–infused rats. In contrast, 100 µmol/L L-NNA constricted afferent arterioles similarly in both control (n=8) and Ang II–infused (n=7) rats. After transection of the loops of Henle to interrupt flow to the macula densa, the vasoconstrictor responses to L-SMTC but not to L-NNA were reversed. Increasing distal volume delivery by addition of 10 mmol/L acetazolamide to the blood perfusate significantly enhanced the afferent arteriolar constrictor responses to 10 µmol/L L-SMTC (34.5±4.8%, n=7) in normotensive rats. In contrast, in Ang II–infused rats, acetazolamide treatment did not enhance the responses to L-SMTC (n=8). These results indicate that chronic Ang II infusion reduces the ability of nNOS-derived nitric oxide to counteract the afferent arteriolar response to increased distal tubular flow.

Key Words: rats • arterioles • macula densa • acetazolamide • papillectomy

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