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Hypertension. 1995;25:898-902

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*Compound via MeSH
*Substance via MeSH
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*(L)-ARGININE
Medline Plus Health Information
*High Blood Pressure

(Hypertension. 1995;25:898-902.)
© 1995 American Heart Association, Inc.


Articles

Effects of L-Arginine Infusion on Renal Hemodynamics in Patients With Mild Essential Hypertension

Yukihito Higashi; Tetsuya Oshima; Ryoji Ozono; Mitsuaki Watanabe; Hideo Matsuura; Goro Kajiyama

From the First Department of Internal Medicine and Department of Clinical Laboratory Medicine, Hiroshima (Japan) University School of Medicine.

Correspondence to Yukihito Higashi, MD, First Department of Internal Medicine, Hiroshima University School of Medicine, 1-2-3 Kasumi, Minami-ku, Hiroshima 734, Japan.

Abstract Previous studies have shown that endothelium-derived relaxing factor/nitric oxide plays an important role in the regulation of systemic and renal hemodynamics. The purpose of the present study was to determine whether endothelium-dependent renovascular relaxation was impaired in patients with mild essential hypertension who had normal renal plasma flow and glomerular filtration rate. We evaluated the effects of intravenous administration of L-arginine on blood pressure and renal hemodynamics in 13 patients with mild essential hypertension and 15 normotensive control subjects. L-Arginine infusion (500 mg/kg over 30 minutes) reduced mean blood pressure (from 82.5±2.5 to 76.3±2.6 mm Hg in hypertensive patients and from 106.1±3.0 to 97.5±2.9 mm Hg in control subjects; P<.001) and renovascular resistance (from 0.084±0.009 to 0.067±0.009 mm Hg · mL-1 · min-1 · [1.48 m2]-1 and from 0.105±0.010 to 0.093±0.011 mm Hg · mL-1 · min-1 · [1.48 m2]-1, respectively; P<.001). L-Arginine infusion increased renal plasma flow (from 602±36 to 698±40 mL · min-1 · [1.48 m2]-1, P<.05) in normotensive subjects but not in hypertensive subjects, and glomerular filtration rate was unaffected in both groups. Although the L-arginine–induced reduction in mean blood pressure was similar in both groups, the decline in renovascular resistance was smaller in hypertensive subjects. The response of renal plasma flow was also smaller in hypertensive subjects. These findings suggest that dysfunction of the L-arginine–nitric oxide pathway exists in the renal circulation even in mild essential hypertension with normal renal plasma flow and glomerular filtration rate. Thus, changes in renal endothelial function could be a cause rather than a consequence of hypertension.


Key Words: arginine • nitric oxide • hypertension, essential • blood pressure • renal circulation




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