Altered responses to 5-hydroxytryptamine in hypertension and other cardiovascular disorders

5-Hydroxytryptamine (5-HT; serotonin) can either cause vasodilatation or vasoconstriction with resulting increases in blood flow and decreases in blood pressure or vice versa [1]. This complexity can be explained by the interaction of the monoamine with different receptors within the vascular wall. On the one hand, activation of endothelial receptors by 5-HT will cause the release of a short-lived vasodilatator substance (EDRF: endothelium derived relaxing factor) and activation of 5-HT receptors on the adrenergic nerve endings will result in a decreased liberation of noradrenaline [2–7]. The receptors involved in these actions of 5-HT leading to vasodilatation belong to the 5-HT1-like type [4, 7–9]. On the other hand, 5-HT can cause vasoconstriction by activation of 5-HT2 receptors on the vascular smooth muscle cells [10–12]. Whether a particular vascular bed will respond to 5-HT with a vasodilatation or a vasoconstriction will ultimately depend upon a balance between factors which determine which of the two receptor systems can play a dominating role. It is the aim of this chapter to specifically review the evidence of pathological changes favouring the 5-HT2 receptor mediated vasoconstriction.