When 5-hydroxytryptamine (5HT) or its analogue, 5-methoxy-α-methyltryptamine (5MOαMT) are added to rat citrated platelet-rich plasma (PRP), the platelets change in shape but do not aggregate. The response to both of these agents is inhibited by the 5HT antagonist, cinanserin (IC50 = 3 व 10-9 M). Cinanserin is at least 10,000 times less potent against the active uptake of 5HT (IC50 > 5 व 10-5 M). 5MOαMT is not actively transported by the platelet, although some instantaneous binding can be measured which is independent of temperature (4°-37°). 5MOαMT does not inhibit 5HT uptake over the concentration range at which it induces the shape change (10-8-10-5 M). Binding of (3H)-5HT to rat platelets at 4° indicates the presence of three binding sites, one of which is specifically blocked by cinanserin (IC50 = 2.8 × l0-9 M). Close correlation between the inhibitory potency of various drugs against (3H)-5HT binding and 5HT-induced shape change suggests that this site is the 5HT receptor on the platelet which initiates the shape change. Our results indicate that 5HT induces the platelet shape change by combination with a specific cinanserinsensitive 5HT receptor, which is unconnected with the uptake site.
Influence of sex and gonadal hormones on rat-liver and carcass lipids during the development of an essential fatty acid deficiency
