Abstract
There have not been as many studies of vascular responsiveness to the platelet activating factor (PAF) as one might expect. The mechanism of PAF's action on blood vessel contractility has not yet been elucidated. In this study, using the isolated perfused arterial segment of the central artery of a rabbit ear and autologous platelets, we examined the effects of PAF on the vasocontractile response to noradrenaline (NA-R).
We obtained the following results: (1) In the absence of platelets, i.e., under the conditions of perfusion with modified normal Krebs' solution alone, PAF (0.036 to 33ng/ml) had no significant influence on NA-R and basal perfusion pressure (BPP); (2) during infusion of platelet rich plasma (PRP) with PAF, NA-R was significantly more augmented, as compared with that during infusion of PRP without PAF; (3) there was no significant difference between BPP during infusion of PRP alone and that during infusion of PRP with PAF; and (4) during infusion of PRP with PAF, NA-R was alleviated by the application of ketanserin, a selective 5-HT2 receptor antagonist, while this response was little influenced by indomethacin, a cyclo-oxygenase inhibitor.
On the basis of these results, it is possible to conclude that PAF acts on blood vessel contractility through platelets, and that 5-HT may, at least in part, participate in augmenting NA-R by PRP with PAF rather than prostanoids.
