Hypertension may result from excessive activity of one or more components of the blood pressure-elevating system. These include the adrenergic nervous system, the renin-angiotensin axis, and mineralocorticoids (aldosterone), which potentiate each other, reinforcing their effects on renal hemodynamics and electrolyte transport and thereby affecting extracellular fluid volume, vascular tone, and reactivity. We consider of no less importance in the genesis of hypertension the failure of one or more components of the blood pressure-lowering system: the kallikrein-kinin system, prostaglandin, or one or more lipids associated with the renomedullary interstitial cells. As a corollary of this hypothesis, if one assumes tonic activity of these opposing blood pressure-regulating systems, in the case of a deficiency of the vasodepressor system, hypertension should result. That is, unopposed activity of the pressor system should be sufficient to increase blood pressure without an increase in the "basal level" of its activity. Hypertension, then, may be considered to result from either uncompensated deficiencies or excesses, which may be relative or absolute, of one or more components of the vasodepressor and vasopressor systems.