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(Hypertension. 1999;33:1008-1012.)
© 1999 American Heart Association, Inc.

Scientific Contributions

Blood Pressure, Sodium Intake, Insulin Resistance, and Urinary Nitrate Excretion

Francesco S. Facchini; Carlos DoNascimento; Gerald M. Reaven; Jeannie W. Yip; Xi Ping Ni; Michael H. Humphreys

From the Division of Nephrology, San Francisco General Hospital, and University of California at San Francisco (F.S.F., C.D., J.W.Y., X.P.N., M.H.H.); Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, Brazil (C.D.); and Division of Endocrinology, Stanford University, Stanford, Calif, and Shaman Pharmaceuticals, Inc, South San Francisco, Calif (G.M.R.).

Correspondence to Michael H. Humphreys, MD, Division of Nephrology, San Francisco General Hospital, Box 1341, University of California at San Francisco, San Francisco, CA 94143-1341. E-mail mhhsfgh{at}itsa.ucsf.edu

Abstract—The objective of this study was to investigate the relationships among various humoral factors thought to be involved in the regulation of blood pressure during high NaCl intake. Nineteen healthy subjects underwent sequential 5-day periods ingesting a low-sodium (25 mmol/d) or high-sodium (200 mmol/d) diet. Insulin resistance was assessed by the steady-state plasma glucose concentration at the end of a 3-hour insulin suppression test. Insulin resistance correlated inversely with natriuresis (P=0.04) and directly with increase in weight (P=0.03). The increase in mean arterial pressure associated with the high-sodium diet correlated directly with the gain in weight (P<0.05) and inversely with the increase in urinary nitrate excretion (P<0.0001). In a multiple regression model, more than 2/3 of the variance in mean arterial pressure was accounted for by the gain in weight and change in urinary nitrate excretion. The steady-state plasma glucose concentrations obtained with the 2 diets were similar, indicating that insulin resistance was unaffected by sodium intake. During high sodium intake, plasma renin activity and aldosterone decreased and plasma atrial natriuretic peptide increased; these changes did not correlate with the change in mean arterial pressure, insulin resistance, or change in urinary nitrate excretion. To the extent that urinary nitrate excretion reflects activity of the endogenous nitric oxide system, these results suggest that the salt sensitivity of mean arterial pressure may be related to blunted generation of endogenous nitric oxide. The results also demonstrate that insulin-resistant individuals have an impaired natriuretic response to high sodium intake.

Key Words: insulin resistance • nitric oxide • sodium chloride, dietary • blood pressure • hypertension, sodium dependent

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