Tryptamine‐induced vasoconstrictor responses in rat caudal arteries are mediated predominantly via 5‐hydroxytryptamine receptors

Abstract

1 It has been suggested that tryptamine can stimulate specific receptors distinct from those for 5-hydroxytryptamine (5-HT). We have examined this possibility in the rat isolated caudal artery, paying particular attention to the involvement of monoamine oxidase metabolism and α-adrenoceptors, two factors that can complicate the quantification of antagonist potencies at 5-HT receptors. 2 5-HT and tryptamine were agonists over the concentration-ranges 3.0 × 10⁻⁸ − 3.0 × 10⁻⁵ moll⁻¹ and 1.0 × 10⁻⁶−3.0 × 10⁻⁴ moll⁻¹ respectively. The sensitivity of the caudal artery to tryptamine was increased by about 44 fold in the presence of iproniazid (5.0 × 10⁻⁵ moll⁻¹) and about 17 fold in the presence of pargyline (1.0 × 10⁻⁵ moll⁻¹), while responses to 5-HT and methoxamine were unaffected. 3 In the absence of iproniazid, ketanserin and methysergide were potent antagonists of responses to 5-HT with pA₂ values of 9.08 and 9.11 and slopes of the Schild regressions of 1.15 and 1.00 respectively. However, against tryptamine the antagonists were weaker such that pA₂ values were similar to those against 5-HT but the slopes of the Schild regressions were 0.47 and 0.47. 4 In the presence of iproniazid (or pargyline), the 5-HT antagonists were more potent against tryptamine such that the pA₂ values and the slopes of the Schild regressions were not significantly different from those against 5-HT. Phentolamine was a weak antagonist of responses to both 5-HT and tryptamine in the presence of iproniazid. 5 The findings in this study suggest that the contractile action of tryptamine in rat caudal artery is mediated predominantly by the same receptor as 5-HT and that the differential inactivation of tryptamine by monoamine oxidase enzymes largely accounts for the different susceptibilities of 5-HT and tryptamine to the antagonists examined.