In hypertension, vasoconstrictor responses to serotonin are augmented while the vasodilator effects of the monoamine are decreased. In animal models of the disease the constrictor response to serotonin is increased more than those to other agonists, which suggests a functional adaptation of the hypertensive blood-vessel wall. In hypertension the turnover of circulating platelets, the major source of peripheral serotonin, is accelerated and the mechanisms for its removal (endothelial metabolism, uptake by platelets) are slower. The functional changes of the blood-vessel wall of the platelets could play a role in the maintenance of the increased peripheral vascular resistance in chronic hypertension. These changes could be involved in the pathogenesis of complications of the hypertensive process. The concept that serotonin plays a role in chronic hypertension is further supported by the antihypertensive properties of the S2-serotonergic antagonist ketanserin.