The sympathetic neurobiology of essential hypertension: Disparate influences of obesity, stress, and noradrenaline transporter dysfunction?

Although the importance of sympathetic nervous activation in the pathogenes is of essential hypertension is well documented, the exact pathophysiology of the sympathetic nervous dysfunction present remains to be delineated. Th is review details three relatively new findings of disturbed sympathetic ne urobiology in hypertension. Adrenaline cotransmission is present in the cardiac sympathetic nerves of p atients with essential hypertension, as it is in patients with panic disord er, providing presumptive evidence of exposure to high levels of mental str ess in hypertensive patients. In lean patients with hypertension there is a lso evidence of faulty noradrenaline reuptake into the sympathetic nerves o f the heart, an abnormality amplifying the sympathetic neural signal by imp airing removal of noradrenaline from the synaptic cleft. If both abnormalit ies are present in the sympathetic nerves of the kidneys also (which we did not test), there would most probably be a direct contribution to hypertens ion development. In the kidneys the causal chain between sympathetic overac tivity and the development of hypertension is stronger than for the heart. In obesity-related hypertension there is evidence that renal sympathetic to ne is high, based on approximately a doubling of the measured rate of spill over of noradrenaline into the renal veins. This increase in sympathetic ou tflow to the kidneys appears to be a necessary but apparently not a suffici ent cause for the development of clinical hypertension, commonly being pres ent also in overweight people with blood pressure in the normotensive range . High renal sympathetic tone in the latter, of course, may well still cont ribute to elevation of their pressure level, although not on such a scale a s to cause clinical hypertension. (C) 2001 American Journal of Hypertension , Ltd.