Actions of Anaphylatoxin on Circulation and Respiration of the Guinea Pig

Bodammer, G.; Vogt, W.

doi:10.1159/000229953

Cited by 40 publications

(27 citation statements)

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“…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).…”

Section: Introductionmentioning

confidence: 99%

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

Hugli

Marceau

1985

British J Pharmacology

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Strips of rabbit blood vessels were suspended in vitro and responses to complement peptides C3a and C5a were recorded isotonically. Human C3a (up to 1.5 μm) was inactive on rabbit vascular strips. Human C5a (2.9–59 nm) decreased spontaneous activity of the rabbit portal vein under resting baseline tension. The C5a relaxed strips of portal vein and pulmonary artery that were precontracted with noradrenaline (NA, 200 nm). On the portal vein, C5a‐induced relaxation was preceded by a transient contractile phase which decreased with repeated applications of C5a. The magnitude of C5a‐induced relaxation of both vessels increased with repeated stimulation by C5a. Maximal levels of relaxation for the third application of C5a at 59 nm averaged 44% and 17% of the NA‐induced contraction plateau in portal vein and pulmonary artery, respectively. Strips of rabbit aorta responded minimally to C5a. Indomethacin (5.6 μm) significantly inhibited C5a‐induced relaxation of the portal vein and pulmonary artery but had no effect on the early contractile response of the portal vein. Mepyramine (10 μm) failed to modify the C5a response from either vessel, but it reduced the contractile phase of the C5a response on the portal vein when applied in conjunction with indomethacin. The drug SKF 88046, an end organ antagonist of thromboxane (TX) A2 and some contractile prostaglandins, reduced the contractile phase and increased relaxation of the portal vein to C5a but did not modify the response of the pulmonary artery. Radioimmunoassays for 6‐keto‐prostaglandin F1α (6‐keto‐PGF1α) and TXB2 were performed on the fluid bathing rabbit isolated blood vessels. C5a promoted release of 6‐keto‐PGF1α over the basal release rate in rabbit tissues. Only trace quantities of TXB2 were produced by rabbit vessels exposed to C5a. It is concluded that the mechanical response of blood vessels to C5a is mainly determined by the type of cyclo‐oxygenase products released and by the sensitivity of each blood vessel to these active lipids. Tissue histamine release is also responsible for a component of the response of rabbit portal vein to C5a. The relaxant effect of C5a on rabbit blood vessels may be a phenomenon related to the previously reported hypotensive action of classical anaphylatoxins in vivo.

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Section: Introductionmentioning

confidence: 99%

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

Hugli

Marceau

1985

British J Pharmacology

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“…On the basis of previous investigations it is well established that the components to be considered are: 1. A direct smooth muscle stimulating activity contributing to the bronchoconstrictor effect Vogt, 1967 andSackeyfio, 1971). 2.…”

Section: Discussionmentioning

confidence: 99%

“…2. Release of histamine (Bodammer & Vogt, 1970) accounting for the major part of the bronchoconstrictor responses and other smooth muscle stimulation, and also leading to a major influence on the cardiovascular system (Bodammer & Vogt, 1967;Sackeyfio, 1971).…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, it has been shown that both histamine and catecholamines are involved in responses to anaphylatoxin (AT) in the guinea-pig (Bodammer & Vogt, 1967;Bernauer, Hahn, Beck & Kury, 1970). But it is not clear whether the ATinduced catecholamine release is entirely a consequence of histamine liberation, or partly due to a direct action of AT on catecholamine-containing tissue (Bodammer & Vogt, 1967;.…”

Section: Introductionmentioning

confidence: 99%

“…But it is not clear whether the ATinduced catecholamine release is entirely a consequence of histamine liberation, or partly due to a direct action of AT on catecholamine-containing tissue (Bodammer & Vogt, 1967;.…”

Section: Introductionmentioning

confidence: 99%

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

Hicks

Sackeyfio

1972

British J Pharmacology

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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.

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Chemistry and biology of the anaphylatoxin related serum peptide system. I. Purification, crystallization and properties of classical anaphylatoxin from rat serum

Wissler

1972

Eur J Immunol

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Chemistry and biology of the anaphylatoxin related serum peptide system* I. Purification, crystallization and properties of classical anaphylatoxin from rat serum" Classical anaphylatoxin, which causes histamine liberation and lethal anaphylatoxin shock in the guinea pig, was purified from dextran-treated rat serum leading t o a 5000-fold increase in specific activity. It was crystallized in a molecular homogenous state. Rat anaphylatoxin consists of one peptide unit with a molecular weight of 9500, as determined by gel chromatography.First, evidence is presented that the anaphylatoxin-forming contact reaction of normal, fresh serum with hydrophilic, insoluble substances of high molecular weight, e.g. dextran, yeast or antigen-antibody complexes, does not lead to a stable anaphylatoxin molecule exclusively, but t o a group of peptides of similar physicochemical behavior. Only one of these peptides displays anaphylatoxin activity. The lack of significant chemotactic activity for neutrophil leucocytes is characteristic for this crystallized classical anaphylatoxin. This indicates that anaphylatoxin and chemotactic activities are two different biological principles. Abbreviations: CAT: Classical anaphylatoxin Complement components: Nomenclature according to Bull. WHO 1968. 39. 935, also given in Immunochernistry 1970. 7: 137 J.H. Wissler Eur. J. Immunol. 1972. 2: 73-83 del-de-Haen, Selze-Hannover, Germany and Fluka AG, Buchs SG., Switzerland. Proteins for column calibration were obtained in the highest purity grade available from Serva, and Sigma, St. Louis, U.S.A. Unless otherwise stated, these chemicals were used throughout. Trasylol (kallikrein inactivator) is a product of Bayer, Leverkusen, Germany. All kinds of Sephadex, Blue Dextran and Dextran 2000 (To. 4386 = 0.70, % , ca. 2 . l o 6 ) were obtained from Pharmacia AB, Uppsala, Sweden.Before use, all Sephadex sorts, especially CM-Sephadex C-50, were treated with hog serum for surface inactivation (minimum incubation time: 1 day).After removal of the excess of protein by rinsing of the gels with tap water, gels were regenerated by successive treatment with 0.1 N HCl and 0.1 N NaOH, as recommended by the seller (flotation method). For purposes of neutralization and for buffer solutions, only double distilled water was used. This is crucial for a successful purification procedure (see also under section 4, 5). Hydroxyapatite was prepared according t o Swingle and Tiselius [27], Hydroxyapatite was separated into crystal particles of homogenous particle size distribution according t o the method of Hamilton [28, 291. Particle size fractions of 5 -10 pm and 10 -I 5 pm in Martin's diameter [30] were obtained and used* throughout. Calcium phosphate gel was synthesized according t o the method of Keilin and Hartree [31]. Only gels of a minimum age of ten weeks were used.

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Actions of Anaphylatoxin on Circulation and Respiration of the Guinea Pig

Cited by 40 publications

References 2 publications

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

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

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

Chemistry and biology of the anaphylatoxin related serum peptide system. I. Purification, crystallization and properties of classical anaphylatoxin from rat serum

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