Effects of High and Low Sodium Intake on Arterial Pressure and Forearm Vascular Resistance in Borderline Hypertension: A Preliminary Report

• Published in: Circulation research 1975-06, Vol.36 (6 Suppl 1), p.I-194-I-198
• Main Authors: Mark, Allyn L, Lawton, William J, Abboud, Francois M, Fitz, Annette E, Connor, William E, Heistad, Donald D
• Format: Article
• Language: English
• ISSN: 0009-7330; 1524-4571
• DOI: 10.1161/01.res.36.6.194

The purpose of this study was to evaluate effects of high and low sodium intake on arterial pressure and forearm vascular resistance in subjects with borderline hypertension and to compare responses to sodium excess in these subjects with responses in a recent study in normotensive subjects. Six subjects with borderline hypertension were studied after ten days of high (410 mEq/24 hr) and low (10 mEq/24 hr) sodium intake. Potassium intake was constant. In five of six subjects, high sodium intake decreased forearm blood flow and increased forearm vascular resistance and arterial pressure. During low and high sodium intake forearm blood flow averaged 7.8 ±1.2 (se) and 5.9 ± 0.8 ml/min x 100 ml, respectively; forearm vascular resistance averaged 13.5 ± 2.2 and 19.1 ± 3.0 units, respectively; and mean arterial pressure averaged 89 ± 3 and 98 ± 2 mm Hg, respectively. High sodium intake augmented forearm vasoconstrictor responses to lower body negative pressure, a stimulus to neurogenic vasoconstriction. The results contrast with our earlier results in normotensive subjects in whom sodium excess produced forearm vasodilatation and failed to increase arterial pressure significantly. Decreases in renin and aldosterone with high sodium intake were similar in the two groups. The results suggest that excessive sodium intake in subjects with borderline hypertension produces abnormal increases in forearm vascular resistance, neurogenic vasoconstriction, and arterial pressure. The reasons for the contrast between the borderline hypertensives and normotensives are unknown, but they do not seem to be related to the renin-angiotensin-aldosterone system.