The acute cardiovascular and respiratory responses of the gulf toadfish, Opsanus beta, to acute hypoxia or exposure to the O(2) chemoreceptor stimulant, sodium cyanide (NaCN) were characterized and the role of serotonin type 2 (5-HT(2)) receptors in mediating these responses was investigated. Toadfish responded to hypoxia or NaCN exposure with a decrease in heart rate (fH) and an increase in breathing amplitude (V(AMP)) but no change in breathing frequency (fR). The bradycardia appeared to be mediated to some extent by 5-HT(2) receptors, as methysergide, a non-selective 5-HT(1/2) receptor antagonist, and ketanserin, a 5-HT(2) receptor antagonist, attenuated the response. Injection of alpha-methyl-5-HT, a 5-HT(2) agonist, also resulted in bradycardia that was inhibited by ketanserin, lending further support for 5-HT(2) receptor involvement, possibly 5-HT(2A) or 5-HT(2C), in the regulation of fH. External NaCN exposure resulted in a significant decrease in caudal arterial blood pressure (P(CA)) that was attenuated by methysergide. In contrast, injection with alpha-methyl-5-HT resulted in a substantial increase in P(CA) that was not affected by ketanserin, suggesting the possible involvement of 5-HT(2B) or 5-HT(2C) receptors. These data are the first to suggest a unique distribution of 5-HT(2B/2C) receptors may be involved in mediating vasoconstriction of the systemic vasculature of toadfish. These data also provide mechanistic support for why pulsatile urea excretion, believed to be regulated by 5-HT via the toadfish 5-HT(2A) receptor, is not triggered by hypoxia or external chemoreceptor activation.