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ABSTRACT The effects of GABA and two inhibitory neuropeptides were tested on the cardiovascular system of intact Cancer magister. A pulsed-Doppler flow meter was used to record heart rate and hemolymph flow rates through each arterial system in C. magister. Summation of arterial flow rates gave a value for cardiac output, and division of this by rate yielded stroke volume of the heart. The insect neuropeptides SchistoFLRFamide and leucomyosuppressin and the neurotransmitter Y-aminobutyric acid (GABA) were infused into the pericardial sinus of the crab so as to achieve final circulating concentrations between 10 12 mol·l1 and 105 mol·l-1. Both SchistoFLRFamide and leucomyosuppressin had similar effects. Neither hormone had an effect on heart rate, but stroke volume was significantly depressed, leading to a decrease in total cardiac output. Hemolymph flow through the sternal artery and anterolateral artery decreased. Effects on flow through the posterior and anterior aortae were slight and variable, while flow through the hepatic arteries remained stable. Threshold for these responses occurred at circulating concentrations of 10 8 mol·l 1 and above, and the effects of SchistoFLRFamide were of longer duration compared with those induced by leucomyosuppressin. These peptides may play a role in digestion during quiescent periods, by diverting hemolymph away from locomotory structures and toward the digestive glands. GABA induced a large bradycardia with related decrease in flows, but induced no differential effects on flow through any arterial system. Effects of GABA were of short duration, with both heart rate and flows recovering quickly after infusion. Effects were seen at circulating concentrations of 10-6 mol·l-1 and above. All these substances are reported to have inhibitory effects on isolated or semi-isolated heart preparations. Inhibition of stroke volume (by the peptides) was seen in the in vivo preparations used here, but heart rate was unaffected. Thus, opposing effects of "cardioactive" hormones, previously reported between in vitro and in vivo preparations is not consistent, and is dependent on the actual hormone and the pathway it acts upon in modulating cardiac activity.


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