Iron overload has been recently shown to be associated with a hyperadrenergic state in
genetic hemochromatosis. Whether this is also the case in
essential hypertension, characterized by sympathetic activation and frequently by body
iron overload, is unknown. In 17 healthy normotensive controls (age 52.3±3.2 years, mean±SE), in 21 age-matched patients with
hypertension with
iron overload (HT+), defined by serum
ferritin levels, and in 28 hypertensives without this condition, we measured efferent postganglionic muscle sympathetic nerve traffic (microneurography), heart rate and blood pressure variability (power spectral analysis), serum
ferritin, and metabolic variables. Muscle sympathetic nerve traffic was significantly (P<0.02 at least) greater in HT+ than in patients with
hypertension without
iron overload and normotensive subjects both when expressed as bursts incidence over time (41.8±1.4 versus 31.5±1.4 and 23.6±0.9 bursts/min) and as bursts corrected for heart rate (55.3±1.8 versus 42.3±1.2 and 31.7±1.2 bursts/100 heartbeats). In HT+, low-frequency systolic blood pressure variability was significantly reduced. In HT+, but not in the other 2 groups, muscle sympathetic nerve traffic was significantly related to serum
ferritin (r=0.51, P<0.03),
transferrin saturation (r=0.47, P<0.03), and hepatic
iron load (r=0.76, P<0.0001, magnetic resonance imaging), as well as to homeostatic model assessment index values (r=0.46, P<0.05). These data provide the first evidence that in HT+
elevated serum ferritin is associated with a hyperadrenergic state of greater magnitude than the one seen in patients with
hypertension without
iron overload. They also show that the potentiation of the sympathetic activation detected in HT+ is related to
elevated serum ferritin and to the associated metabolic alterations, possibly participating in the increased cardiovascular risk characterizing
iron overload.