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Catecholamines released from the adrenal medulla exert a compensatory, protective effect at β 2 ‐adrenoceptors against Paf‐induced death in mice

1988; Wiley; Volume: 93; Issue: 1 Linguagem: Inglês

10.1111/j.1476-5381.1988.tb11413.x

1476-5381

Marco Criscuoli, Alessandro Subissi,

Asthma and respiratory diseases

The effects of a number of drugs and experimental conditions, which inhibit or stimulate adrenergic function, were evaluated on platelet‐activating factor (Paf)‐induced death in conscious mice. Adrenalectomy markedly potentiated Paf toxicity, while guanethidine and reserpine did not. However, reserpine, which produced a virtually complete depletion of cathecolamines (CA) in cardiac tissue, was not able to reduce adrenal CA by more than 58%. Drugs which release noradrenaline from the adrenergic nerve terminals, such as tyramine and amphetamine, did not protect mice from Paf toxicity, while drugs or conditions which favour the release of CA from the adrenal medulla, such as urethane and cold‐induced stress, did. β 2 ‐ and β 1 + β 2 ‐adrenoceptor antagonists (ICI 118551, propranolol and nadolol), but not β 1 ‐ antagonists (atenolol, practolol, metoprolol and CGP 20712 A), potentiated Paf toxicity at low doses; β 2 ‐ and β 1 + β 2 ‐agonists (salbutamol, fenoterol and isoprenaline), but not β 1 ‐agonists (prenalterol and tazolol) were potent inhibitors of Paf toxicity. α 1 ‐ and α 2 ‐adrenoceptor agonists and antagonists did not exert significant effects. Propranolol did not appear to enhance the hypotensive action of Paf in pentobarbitone‐anaesthetized mice. It is concluded that manipulation of the release of CA from the adrenal medulla, but not from adrenergic nerves, has profound effects on Paf toxicity in mice. A number of considerations support the hypothesis that bronchoconstriction is a major determinant of Paf‐induced death in mice.