Amplifying Effect of Serotonin in the Control of Vascular Tone

Threshold or subthreshold concentrations of serotonin, either exogenously applied or released from aggregating platelets, amplify the vasoconstriction caused by low concentrations of neurohumoral mediators in large or small arteries. This amplifying effect of serotonin is larger than would be expected from a merely additive effect. In most blood vessels it can be inhibited by 5HT2-serotonergic antagonists such as ketanserin, indicating that 5HT2- serotonergic receptors are involved. The amplifying effect may be enhanced at older age or in hypertension. The amplification is relatively more important at lower concentrations of the agonists. When the uptake or storage of serotonin in blood platelets is impaired, or when platelets aggregate, the low amounts of serotonin then present in the plasma may cause vasospasms because of the amplifying effect of the monoamine. The findings that the 5HT2-serotonergic antagonist ketanserin improves blood flow in atherosclerotic animals or in thrombotic obstruction and that it lowers high blood pressure suggests that the amplifying effect of serotonin may play a role in cardiovascular pathology.