The aim of the present study was to further investigate the cardiovascular activity
of Pterois volitans crude venom. Venom (0.6-18 microg protein/ml) produced dose- and
endothelium-dependent relaxation in porcine coronary arteries that was potentiated
by atropine (10nM), but significantly attenuated by the nitric oxide synthase inhibitor
N(omega)-nitro-L-arginine (NOLA; 0.1mM), by prior exposure of the tissue to stonefish
antivenom (SFAV, 3 units/ml, 10 min), or by removal of extracellular Ca(2+). In rat
paced left atria, venom (10 microg protein/ml) produced a decrease, followed by an
increase, in contractile force. Atropine (0.5 microM) abolished the decrease in force
and potentiated the increase. Propranolol (5 microM) did not affect the decrease in
force but significantly attenuated the increase. In spontaneously beating right atria,
venom (10 microg protein/ml) produced an increase in rate that was significantly attenuated
by propranolol (5 microM). Prior incubation with SFAV (0.3 units/microg protein, 10
min) abolished both the inotropic and chronotropic responses to venom. In the anaesthetised
rat, venom (100 micro protein/kg, i.v.) produced a pressor response, followed by a
sustained depressor response. Atropine (1mg/kg, i.v.) potentiated the pressor response.
The further addition of prazosin (50 microg/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).
Copright 2002 Elsevier Science Ltd.