Cardiac adrenoceptors at low temperature and the adrenoceptor interconversion hypothesis

Abstract

1The hypothesis that low temperature converts inotropic,-adrenoceptors to a-adrenoceptors has been tested in isolated heart preparations of the frog and rat. 2 The results do not support the adrenoceptor interconversion hypothesis. In the frog ventricle strip lowering the temperature from 240C to 140C did not significantly alter the inotropic potency of the sympathomimetic drugs isoprenaline, adrenaline and phenylephrine and did not reduce the potency of the J-adrenoceptor blocking drug propranolol as an isoprenaline antagonist. In the isolated left atrium of the rat lowering the temperature from 31 IC and 24°C to 17-190C did not significantly alter the inotropic potency of isoprenaline, noradrenaline and phenylephrine, did not diminish the potency of the f-adrenoceptor blocking drug propranolol and did not increase the potency of the a-adrenoceptor blocking drug phentolamine.3 Phenylephrine acted on a-and fl-adrenoceptors in rat left atrium at 31°C and 24°C, but only on fiadrenoceptors at 17-19°C.

Polymethylene tetraamines: A novel class of cardioselective M2‐antagonists

“…26 The design of tetraamines as muscarinic receptor antagonists was based mainly on the observation that the disulfide moiety, contrary to the situation at a-adrenoreceptors, is not necessary for the antimuscarinic action of benextramine since its replacement by two methylenes did not modify the biological profile towards cholinergic receptors ( Fig. 2).u,"* 25 The fact that polymethylene tetraamines with suitable substituents on the nitrogens (see below) retain antimuscarinic properties while losing affinity for a-adrenoreceptors indicates that muscarinic receptors and c&adrenoreceptors are inhibited by two different mechanisms.…”