The sympathetic system and hypertension

Measurement of regional sympathetic activity in lean essential hypertension patients using electrophysiologic (sympathetic nerve recording) and neuroc hemical (measurement of norepinephrine spillover) techniques demonstrates a ctivation of sympathetic outflow to the heart, kidneys, and skeletal muscle vasculature in younger (< 45 years) patients. The increase in sympathetic activity is a mechanism for both initiating and sustaining the blood pressu re elevation. Sympathetic nervous activation also confers specific cardiova scular risk. Stimulation of the sympathetic nerves to the heart promotes th e development of left ventricular hypertrophy and contributes to the genesi s of ventricular arrhythmias and sudden death. Sympathetically mediated vas oconstriction in skeletal muscle vascular beds reduces the uptake of glucos e by muscle, and is thus a basis for insulin resistance and consequent hype rinsulinemia. Understanding the neural pathophysiology of obesity-related h ypertension has been more difficult. In normotensive obesity, renal sympath etic tone is doubled, but cardiac norepinephrine spillover (a measure of sy mpathetic activity in the heart) is only 50% of normal. In obesity-related hypertension, there is a comparable elevation of renal norepinephrine spill over, but without suppression of cardiac sympathetics, as here cardiac nore pinephrine spillover is more than double that of normotensive obese and 25% higher than in healthy volunteers. Increased renal sympathetic activity in obesity may be a necessary cause for the development of hypertension (pred isposing to hypertension development), but apparently is not a sufficient c ause. The discriminating: feature of the obese who develop hypertension is the absence of the presumably adaptive suppression of cardiac sympathetic o utflow seen in the normotensive obese. The sympathetic nervous system has moved towards center stage in cardiovasc ular medicine. The importance of sympathetic activation in heart failure pr ogression and mortality and in the generation of ventricular arrhythmias is now well established. In essential hypertension also, although the mechani sm differs somewhat between the lean and obese, the sympathetic nervous sys tem is a key factor in the genesis of the disorder, and additionally promot es the development of complications. Through their central inhibition of sy mpathetic nervous activity, I, agents such as rilmenidine powerfully reduce sympathetic nervous activity in essential hypertension patients, lowering blood pressure, and carrying the potential for specific cardiovascular prot ection. (C) 2000 American Journal of Hypertension, Ltd.