Autonomic nervous system abnormality, clinically manifested as a hyperkinetic circulation characterized by elevations in heart rate, blood pressure, plasma norepinephrine levels, and cardiac output, has been repeatedly demonstrated in hypertension. Increased release of norepinephrine from the brain has also been described in hypertension, and increased sympathetic activity has been demonstrated using spectral analysis of heart rate variability, particularly in the early stage of hypertension and in white-coat hypertension. Studies performed with microneurographic assessment also have found a marked increase in muscle sympathetic nervous activity in subjects with both borderline and established hypertension. A transition from the early hyperkinetic state to a high-resistance, established hypertension has been documented in longitudinal studies. The high blood pressure induces vascular hypertrophy, which in turn leads to increased vascular resistance. Cardiac output returns from elevated to normal values as β-adrenergic receptors are downregulated and stroke volume decreases. In parallel with the hemodynamic transition, the sympathetic tone is reset in the course of hypertension. Autonomic nervous system abnormality is also associated with such pressure-unrelated cardiovascular risk factors as tachycardia, high hematocrit, insulin resistance, and obesity. Mechanisms of this association are discussed.