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PubMed1985

The sympathomimetic activity of (+/-)-pindolol at beta 1- and beta 2-adrenoceptor sites.

In isolated right atrial and stilboestrol-pretreated uterine preparations from both guinea-pigs and rats, pindolol elicited propranolol-sensitive positive chronotropic and smooth muscle relaxant actions. Although the pD2 values for pindolol (8.4-9.2) and (-)-isoprenaline (ISO, 8.4-8.7) fell within the same range in these preparations, the maximum responses to pindolol were less than 15% of those to the catecholamine. Thus, pindolol did not display any selectivity for agonistic actions at beta 1- or beta 2-adrenoceptors. In uteri taken from progesterone-pretreated rats, the pD2 value for (-)-isoprenaline was 9.5 and that of pindolol 8.5. In these preparations the maximal relaxant effect of pindolol (approximately 50% Emax ISO) was greater than that found in oestrogen-pretreated uteri. Thus, it appears that the maximal response of pindolol in vitro can be related to the pD2 value for (-)-isoprenaline. In anesthetized cats, intravenous pindolol elicited non-beta-adrenoceptor-mediated increases in heart rate and decreases in soleus muscle contractility. The mechanism(s) underlying the latter actions are unknown.

Anesthesia↗
PubMed1996

Phenylethylamine and tyramine are mixed-acting sympathomimetic amines in the brain.

On the helical strip of a capacitance vessel, the pulmonary artery of the rabbit, phenylethylamine (PEA) and tyramine act solely via displacement of noradrenaline from their storage sites and this effect is inhibited by desmethylimipramine (DMI). In contrast, on a resistance vessel, the perfused central ear artery of the rabbit, PEA enhances stimulation induced contractions in 0.2-0.8 microgram/ml concentration [catecholaminergic activity enhancer (CAE) effect], and increases smooth muscle tone (noradrenaline displacing effect) in 4-6 micrograms/ml concentration. This latter effect only is blocked by DMI. Tyramine acts similarly and is more potent than PEA. On the isolated brain stem PEA, tyramine and (-)methamphetamine are, in the presence of cocaine and DMI, highly potent enhancers of stimulation induced release of 3H-noradrenaline, 3H-dopamine and 3H-serotonin. Compounds with specific CAE effect in the brain, (-)deprenyl and 1-phenyl-2-propylaminopentane [(-)PPAP], antagonize tetrabenazine-induced depression of performance of rats in the shuttle box. PEA and tyramine, which are rapidly metabolized in vivo, are ineffective in this test up to 40 mg/kg, whereas (-)methamphetamine, the stable PEA derivative, is highly effective. Compounds with CAE effect enhance at low concentrations the slow inward Ca2+ current in the sino-auricular fibers of the frog heart and inhibit it in high concentration. PEA and tyramine enhance Ca2+ influx from 0.05 to 4 micrograms/ml and inhibit it in 8 micrograms/ml. In conclusion, PEA and tyramine stimulate primarily coupling of action potential to transmitter release in the catecholaminergic neurons in the brain and displace catecholamines in higher concentration only.

Animals↗