Adrenergic and cholinergic activity contributes to the cardiovascular effects of lionfish (Pterois volitans) venom

The aim of the present study was to further investigate the cardiovascular activity of Pterois volitans crude venom. Venom (0.6-18 mug protein/ml) produced dose- and endothelium-dependent relaxation in porcine coronary arteries that was potentiated by atropine (10 nM), but significantly attenuated by the nitric oxide synthase inhibitor N-omega-nitro-L-arginine (NOLA; 0.1 mM) by prior exposure of the tissue to stonefish antivenom (SFAV, 3 units/ml, 10 min), or by removal of extracellular Ca2+. In rat paced left atria, venom (10 mug protein/ml) produced a decrease, followed by an increase. in contractile force. Atropine (0.5 muM) abolished the decrease in force and potentiated the increase. Propranolol (5 muM) did not affect the decrease in force but significantly attenuated the increase. In spontaneously beating right atria, venom (10 mug protein/ml) produced an increase in rate that was significantly attenuated by propranolol (5 muM). Prior incubation with SFAV (0.3 units/mug protein, 10 min) abolished both the inotropic and chronotropic responses to venom. In the anaesthetised rat, venom (100 mug protein/kg, i.v.) produced a pressor response, followed by a sustained depressor response. Atropine (1 mg/kg, i.v.) potentiated the pressor response. The further addition of prazosin (50 mug/kg, i.v.) restored the original response to venom. Prior administration of SFAV (100 units/kg, i.v., 10 min) significantly attenuated the in vivo response to venom. It is concluded that P. volitans venom produces its cardiovascular effects primarily by acting on muscarinic cholinergic receptors and adrenoceptors. As SFAV neutralised many of the effects of P. volitans venom. we suggest that the two venoms share a similar component(s). (C) 2002 Elsevier Science Ltd. All rights reserved.