Diminished Forearm Arteriolar Dilator Capacity Produced by Mineralocorticoid-Induced Salt Retention in Man

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Abstract
The mechanism of the increased stiffness of peripheral vessels in patients with congestive heart failure (CHF) is unknown. It was considered that an increased sodium (Na + ) content of peripheral vessels, shown in experimental CHF, might lead to diminished arteriolar dilator capacity. Thus, Na + retention was induced in six normal volunteers by the daily oral administration of 0.2 mg of fludrocortisone acetate (F) and 10 g NaCl for 1 week. This induced a weight increase of 3.1 lb and increased serum Na + and decreased serum potassium concentrations ( P < 0.02). The peak reactive hyperemia blood flow (RHBF) was measured plethysmographically in the forearm before and after treatment. Upon restoration of the circulation after 1, 5, and 10 min of ischemia the peak RHBF was 21.8, 33.1, and 34.9 ml/min/100 ml before administration of F and NaCl but was reduced to 19.6 ( P > 0.2), 28.6 ( P < 0.02), and 24.4 ( P < 0.02) ml/min/100 ml by treatment. Thus, steroid-induced salt retention leads to diminished vascular compliance. Furthermore, it is suggested that increased vascular Na + content is causally related to the vascular stiffness abnormality characterostic of CHF.