A low concentration of serotonin (3 nmol/L), which did not exert a direct vasoconstrictor action, amplified the responses to certain other vasoconstrictor agents (alpha 1-adrenoceptor agonists, KCl, ATP and vasopressin) in isolated perfused segments of the rat tail artery. 2. Low concentrations of serotonin (0.3 and 1 nmol/L) amplified vasoconstrictor responses to sympathetic nerve stimulation, but higher concentrations of serotonin (10 and 30 nmol/L) produced vasoconstriction and reduced responses to sympathetic nerve stimulation. 3. The calcium channel blocking drug diltiazem (1 and 10 mumol/L) produced concentration-dependent reductions of vasoconstrictor responses to phenylephrine. The amplifying effect of serotonin on responses to phenylephrine was attenuated by 1 mumol/L and abolished by 10 mumol/L diltiazem, and was also abolished in a Ca2+-free medium. 4. Ketanserin (10 nmol/L) antagonized the vasoconstrictor action of serotonin and, to a lesser extent, the vasoconstrictor actions of phenylephrine and noradrenaline. It abolished the amplifying effect of a low concentration of serotonin on responses to noradrenaline and phenylephrine. 5. The amplification of vasoconstrictor response in the rat tail artery by serotonin appears to be due to activation of receptors of the 5-HT2 subtype which are coupled to an increase in Ca2+ influx into the vascular smooth muscle cells.
