The effects of adenyl compounds on the heart of the axolotl (Ambystoma mexicanum).

In the spontaneously beating axolotl atrium, adenosine 5'-triphosphate (ATP) produced initial excitation followed by inhibition and then by a secondary excitation. This third phase of the ATP response was only seen in electrically driven preparations in the presence of 8-phenyltheophylline (8-PT), an adenosine receptor antagonist. alpha,beta-Methylene ATP (APCPP), a stable analogue of ATP, produced only excitatory effects, while adenosine and beta,gamma-methylene ATP (APPCP), a slowly degradable ATP analogue, produced inhibition or inhibition followed by excitation. 2-Chloroadenosine produced inhibition. The excitatory effects were not antagonized by 8-PT, indomethacin or propranolol and phentolamine. The negative inotropic responses of these compounds were antagonized by 8-PT and, with the exception of 2-chloroadenosine, potentiated by dipyridamole, an adenosine uptake blocker. In the ventricle, ATP, APCPP and APPCP produced positive inotropic effects, which were not affected by 8-PT, indomethacin or propranolol and phentolamine. Adenosine produced a negative inotropic effect which was not antagonized by 8-PT nor atropine nor potentiated by dipyridamole. The effects of adenyl compounds on the axolotl (urodele) heart suggest that, like the frog (anuran) heart, both P1- and P2-purinoceptors are present in the axolotl atrium and that only P2-purinoceptors are present in the axolotl ventricle, although adenosine does produce an inhibitory effect on the ventricle which is probably mediated via the release of a neurotransmitter other than acetylcholine.