Article date: October 1972
By: R. HICKS, A. C. SACKEYFIO in Volume 46, Issue 2, pages 260-269
. Evidence is presented to elucidate the nature of the adrenergic mechanisms involved in responses of the guinea‐pig to anaphylatoxin (AT).
. Investigation by means of adrenalectomy, adrenergic neurone blockade, α‐ and β‐ adrenoceptor blockade and exclusion of autonomic reflexes, revealed that the adrenergic mechanisms provoked included catecholamine release from the adrenal medulla, sympathetic reflex activity, stimulation of adrenergic neurones and α‐ and β‐adrenoceptor activity.
. The cardiovascular effects of AT, mediated by histamine release, were largely attributable to adrenal medullary and adrenergic neuronal mechanisms. These mechanisms also exerted a restraint on the predominantly histamine mediated bronchoconstrictor effect of AT.
. The cardiovascular effects of AT activity, not attributable to histamine release, were also probably associated with catecholamine release. However, the bronchoconstrictor component of this AT activity was not significantly affected by guanethidine, and it would, therefore, appear that neuronal bronchodilator mechanisms did not exert a restraint upon this aspect of AT activity.
. These findings are generally compatible with previous work showing that adrenergic mechanisms operate during AT‐induced responses. In contrast to previous reports, however, the adrenergic activity was predominantly associated with the effects of released histamine.
. Evidence is presented to elucidate the nature of the adrenergic mechanisms involved in responses of the guinea‐pig to anaphylatoxin (AT).
. Investigation by means of adrenalectomy, adrenergic neurone blockade, α‐ and β‐ adrenoceptor blockade and exclusion of autonomic reflexes, revealed that the adrenergic mechanisms provoked included catecholamine release from the adrenal medulla, sympathetic reflex activity, stimulation of adrenergic neurones and α‐ and β‐adrenoceptor activity.
. The cardiovascular effects of AT, mediated by histamine release, were largely attributable to adrenal medullary and adrenergic neuronal mechanisms. These mechanisms also exerted a restraint on the predominantly histamine mediated bronchoconstrictor effect of AT.
. The cardiovascular effects of AT activity, not attributable to histamine release, were also probably associated with catecholamine release. However, the bronchoconstrictor component of this AT activity was not significantly affected by guanethidine, and it would, therefore, appear that neuronal bronchodilator mechanisms did not exert a restraint upon this aspect of AT activity.
. These findings are generally compatible with previous work showing that adrenergic mechanisms operate during AT‐induced responses. In contrast to previous reports, however, the adrenergic activity was predominantly associated with the effects of released histamine.
DOI: 10.1111/j.1476-5381.1972.tb06871.x
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