Adrenergic Activity and Peripheral Hemodynamics in Relation to Sodium Sensitivity in Patients with Essential Hypertension

In 25 outpatients with essential hypertension, sodium sensitivity, defined as the difference in mean arterial pressure (AMAP) between 2 weeks of high-sodium (300 mmol per day) and 2 weeks of low-sodium (LS) intake (50–100 mmol per day), was studied in relation to the plasma norepinephrine (NE) level, NE release, and pressor response to intravenous NE. In addition, forearm blood flow (FBF) was measured by plethysmography. There were two control periods of regular sodium intake, one of 4 weeksʼ duration at the beginning of the study and one of 2 weeksʼ duration at the end. The AMAP ranged from +18 to − 8 mm Hg. The eight patients in whom AMAP was greater than 10 mm Hg were regarded as salt-sensitive. When compared with salt-insensitive subjects, saltsensitive patients had higher plasma NE levels in the control period (p < 0.05) and after 2 weeks of HS intake (p < 0.01). Sodium sensitivity was directly related to the change in plasma NE between the HS and LS periods (p < 0.001). The NE release decreased in salt-insensitive subjects whereas it increased in salt-sensitive patients between the LS and HS periods. Changes in NE release were directly related to sodium sensitivity (p < 0.05). The pressor response to NE was not significantly influenced by changes in sodium intake. The FBF fell in salt-sensitive patients and increased in salt-insensitive subjects between the LS and HS periods. Sodium sensitivity was directly related to the change in forearm vascular resistance (p < 0.01). Our data indicate that changes in adrenergic activity and in vascular resistance contribute significantly to sodium sensitivity.