Sympathetic drive can contribute not only to the acute adjustment to circulatory stresses but also to sustained elevation in vascular resistance and arterial pressure. In hypertensive animals and humans excessive sympathetic activity coupled with a possible genetic factor may result in defects in electrogenic ion transport of vascular muscle or in excessive vascular hypertrophy. Increased sympathetic activity and release of the neurotransmitter may occur as a result of defects of the efferent, afferent or central components of the sympathetic system. Several studies in various animal models and in humans are described to support the notion that the mosaic concept in hypertension may be embodied in a dual theory that includes a vascular muscle defect coupled with excessive sympathetic drive both of which may be of genetic or acquired origin. Almost regardless of the cause of hypertension, interruption of sympathetic efferent activity lowers arterial pressure.