Until recently the possible role of vasodilator systems in the etiology of hypertension has been largely ignored, although deficiency of vasodilator influence could be more important than the presence of vasoconstriction in determining vascular tone. Lower concentrations of urinary kallikrein excretion have been widely indicated in clinical and in several experimental hypertensive situations. The reduced plasma kininogen levels may reflect either decreased synthesis compensating for a chronically reduced kinin generation or genetic abnormality leading to reduced plasma kininogen, which may be a predisposing factor in hypertension. An alternative possibly could be enhanced adrenergic control during hypertensive conditions which may cause reduction in prostaglandin and kallikrein-kinin systems. It has also been suggested that most of the pharmacological actions of the kallikrein-kinin system are mediated through prostaglandin formation. Thus, subnormal kallikrein-kininogen-kinin concentrations could be the cause of reduced vasodilating influence leading to both clinical and experimental hypertension.