Does mineralocorticoid-induced salt retention reduce forearm arteriolar dilator capacity in normal volunteers?
Mineralocorticoid-induced salt retention diminishes forearm arteriolar dilator capacity, suggesting a mechanism for the vascular stiffness seen in congestive heart failure.
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 0.2), 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.
Zelis et al. (1970) studied this question.