Abstract
As shown previously, adenosine and the adenine nucleotides cause a rapid increase in heart rate (f(H)) and haemolymph velocity (v(HL)) when infused into intact American lobster (Homarus americanus). Here we compare the effects of adenosine and adenine nucleotides on different heart preparations in order to gain insight into their sites of action. In the semi-isolated (in situ) heart preparation where the heart is uncoupled from neural and hormonal influence AMP, ADP and ATP, but not adenosine increased contractile force. None of the purines altered f(H). Thus, the adenine nucleotides directly affect the myocardium and not the f(H)-setting cardiac ganglion. In cardioregulatory-denervated animals in which the cardiac ganglion only was severed from the central nervous system (CNS), purines caused a small and gradual increase in f(H), indicating that in vivo an alteration of f(H) arises indirectly through the central nervous system which in turn sends the information to the heart via the dorsal nerves. The gradual increase in f(H) of cardioregulatory-denervated animals may also result from neurohormones released into the circulatory system, although no significant changes in haemolymph concentration of dopamine, serotonin and octopamine were found during adenosine infusion. In semi-isolated (in situ) hearts adenine nucleotides also increased haemolymph flow, as a consequence of increased heart contractile force, but again adenosine had no effect. These data show that in vivo adenosine does not influence the myocardium, only the adenine nucleotides affect the myocardium directly. Obviously adenosine possesses an indirect effect, perhaps on cardio-arterial valves and arterial resistance, but other, as yet unidentified, modifying factors are also possible.
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