The level of arterial pressure in an individual is dictated by many in
teracting factors including neurohormonal systems. Heightened activity
of presser systems could contribute to the pathogenesis of essential
hypertension; evidence for this is strongest for sympathetic overactiv
ity in some young patients. Inadequacy of vasodilator systems, especia
lly natriuretic peptides or nitric oxide, has also been suggested as c
entral to the pathogenesis of essential hypertension although evidence
is far from definitive. The existence of authentic ouabain in human p
lasma, let alone its pathophysiological importance in hypertension, is
now in doubt. Information is awaited regarding the role of the endoth
elins and adrenomedullin in physiology and in essential hypertension.