(Hypertension. 1996;27:643-648.)
© 1996 American Heart Association, Inc.
Articles |
From the First Department of Internal Medicine and the Department of Clinical Laboratory Medicine (T.O.), Hiroshima University School of Medicine, Hiroshima, Japan.
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 This study examined whether disturbances in nitric oxide formation contribute to renal dysfunction in salt-sensitive essential hypertensive patients. We evaluated the effects of intravenous administration of L-arginine (500 mg/kg given over 30 minutes) on systemic and renal hemodynamics in 23 patients with mild essential hypertension during 1 week of a low NaCl diet (50 mmol/d) followed by 1 week of a high NaCl diet (340 mmol/d). Patients were classified as salt sensitive (n=10) or salt resistant (n=13) based on salt-induced changes in their blood pressures. Salt loading increased renal vascular resistance but not renal plasma flow in salt-sensitive patients. The L-arginineinduced renovascular relaxation was significantly reduced by a high NaCl diet (renal vascular resistance: low NaCl -12.4±2.3% versus high NaCl -7.1±1.8%, P<.001) in salt-sensitive patients, whereas it was unchanged in salt-resistant patients. The increase in plasma cGMP in response to L-arginine was also reduced by a high NaCl diet in the salt-sensitive patients (low NaCl 49±7% versus high NaCl 36±8%, P<.05) but not in the salt-resistant patients (low NaCl 51±6 versus high NaCl 58±6%). These findings suggest that NaCl loading in salt-sensitive patients with mild essential hypertension reduces the ability of L-arginine to produce nitric oxide in the endothelium of the renal vasculature.
Key Words: L-arginine nitric oxide cyclic GMP hypertension, sodium-dependent blood pressure renal circulation
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