Purpose: To investigate the possible role of endothelial mediators on the increased vasoconstriction to 5-HT1 receptor stimulation by the host-modified arterioles feeding a Meth-A tumour implanted in the flank of female Balb/c mice.
Materials and methods: Using intravital microscopy, the response to the topical administration of the general 5-HT1 agonist 5-carboxamidotryptamine maleate (5-CT; 10(-6) M to 10(-4) M) by the tumour-feeding arterioles with the responses of tumour-independent arterioles and those of control arterioles from mice without tumour after antagonization or inhibition of the synthesis of endothelial mediators was compared.
Results: The dramatically higher vasoconstriction to 5-CT observed in tumour-feeding arterioles than in tumour-independent or control arterioles still persisted when either nitric oxide synthase, cyclooxygenase, lipoxygenase, or phospholipase A2 were inhibited or when thromboxane A2 or endothelin were antagonized.
Conclusions: It was concluded that the higher reactivity to 5-HT1 stimulation by tumour-feeding arterioles is not due to changes in endothelial mediator release but probably due to changes affecting arteriolar smooth muscle.