The nature of adrenergic mechanisms involved in anaphylatoxin activity in the guinea‐pig

Abstract

Summary1. Evidence is presented to elucidate the nature of the adrenergic mechanisms involved in responses of the guinea-pig to anaphylatoxin (AT). 2. Investigation by means of adrenalectomy, adrenergic neurone blockade, aand /8-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 a-and /3-adrenoceptor activity.3. 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. 4. 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. 5. 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.

Effects of the C5a anaphylatoxin and its relationship to cyclo‐oxygenase metabolites in rabbit vascular strips

“…That this peptide is the 'classical the guinea-pig and in the dog. A reversible hypotensive anaphylatoxin' C5adesArg is now well established phase followed by a tachyphylactic, catecholaminedependent hypertensive phase was observed in the 'To whom correspondence should be sent guinea-pig after intravenous injection of classical ©The Macmillan Press Ltd 1985 anaphylatoxin (Bodamer & Vogt, 1967;Hicks & Sackeyfio, 1972). In the dog, CSadesArg reduced systemic arterial blood pressure but caused pulmonary hypertension (Pavek et al, 1979).…”

“…A serum carboxypeptidase becomes broncoconstrictive and vasoactive (see Bor-removes the C-terminal arginine residue from anadet, 1913; Hicks & Sackeyfio, 1972). Complex phylatoxins C3a, C4a and C5a when generated in vivo; cardiovascular responses to a peptide purified from but only the C5a molecule retains significant activity complement-activated hog serum were reported in the in the des-Arg form.…”

Systemic and lung physiological changes in rats after intravascular activation of complement

“…Similar hemodynamic responses have been seen in dogs intravenously injected with yeast-activated porcine serum (16). Mediators implicated in these responses include histamine, prostanoids, and catecholamines (3,10,16). Much of this work must be interpreted with care, inasmuch as the infusion of activated serum and, in particular, xenogeneic serum suggests that these adverse responses may, in part, reflect complement-dependent acute vascular damage induced by natural IgM antibody reacting with epitopes on endothelial cells.…”