Haemodynamic aspects and serotonin.

Serotonin (5-HT) induced a transient decrease followed by an increase and then a longer-lasting decrease in blood pressure. The initial decrease in blood pressure results from a reduction in cardiac output as a result of the profound bradycardia. The secondary increase in blood pressure is caused by an increase in both cardiac output and total peripheral resistance. The final decrease in blood pressure is ascribed to a reduction in total peripheral resistance. The effects of 5-HT on regional haemodynamics are known to vary according to the vascular bed and even in the same vascular bed. Accordingly, 5-HT induced either vasoconstriction or vasodilatation. Vasoconstriction occurred in most cases in large arteries and is due to stimulation of 5-HT2 receptors. However, 5-HT1-like receptors are probably also implicated. 5-HT-induced vasodilatation is attributed to stimulation of 5-HT1-like receptors. However, limited evidence suggests also an implication of 5-HT3 and even 5-HT2 receptors in the dilator effects of 5-HT. 5-HT1A receptor agonists decreased blood pressure by a reduction in total peripheral resistance. This vasodilatation seems to be widespread. Other 5-HT1-like receptor agonists have differential effects according to the animal species used.