Interrelationship of cyclic nucleotides and anaphylactic reactions

Coulson, Christopher J.; Ford, R. E.; Marshall, Stuart; Walker, Joyce L.; Wooldridge, K. R. H.; Bowden, Keith; Coombs, Tim

doi:10.1038/265545a0

Cited by 40 publications

(18 citation statements)

References 25 publications

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“…These various observations led to the concept that increases in cyclic AMP reduce mediator release and increases in cyclic GMP enhance release. However, Coulson, Ford, Marshall, Walker, Wooldridge, Bowden & Coombs (1977) showed that the inhibition of immunological histamine release from human lung and passive cutaneous anaphylaxis in the rat were correlated to the relative ability of drugs to inhibit cyclic GMP-hydrolysis. The observation that M&B 22948, a selective inhibitor of cyclic GMP phosphodiesterase (Table 1) rolysis (Schwabe, Miyake, Ohga & Daly, 1976 and Table 1), has no effect on the histamine release from mast cells.…”

Section: Discussionmentioning

confidence: 99%

“…M&B 22948 was indeed introduced as an inhibitor of reagin-mediated anaphylaxis (Broughton, Chaplen, Knowles, Lunt, Pain, Wooldridge, Ford, Marshall, Walker & Maxwell, 1974). Similarly ICI 74917 inhibits immediate hypersensitivity reactions (Evans & Thomson, 1975), and selectively inhibits cyclic GMP hydrolysis (Coulson et al, 1977;Ruckstuhl & Landry, 1981). It must also be noted that DSCG is a highly selective inhibitor of cyclic GMP hydrolysis (Bergstrand, Kristofferson, Lundquist & Schurmann 1977;and Table 1) and has been previously shown to inhibit histamine release from mast cells but not from basophils (Assem & Mongar, 1970).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Effects of Cyclic Amp‐ and Cyclic Gmp‐phosphodiesterase Inhibitors on Immunological Release of Histamine and on Lung Contraction

Frossard¹,

Landry²,

Pauli³

et al. 1981

British J Pharmacology

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Cyclic adenosine 3′, 5′‐monophosphate (cyclic AMP)‐ and cyclic guanosine 3′, 5′‐monophosphate (cyclic GMP)‐phosphodiesterase activities from rat lung were selectively inhibited by ZK 62711 and M & B 22948, respectively. Theophylline and papaverine inhibited both activities. Rat lung strips contracted by carbachol were relaxed by 4‐(3‐cyclopentyloxy‐4‐methoxyphenyl)‐2‐pyrrolidone (ZK 62711, EC25 = 7 × 10−8m) and 2‐O‐propoxyphenyl‐8‐azapurin‐6‐one (M&B 22948, EC25 = 5 × 10−7m) indicating relaxant properties of both cyclic AMP and cyclic GMP. The antigen‐induced histamine release from human basophils was inhibited by ZK 62711 (IC25 = 8 × 10−7m), whereas M&B 22948 had no effect. On the contrary, the release from rat mast cells was inhibited by M&B 22948 (IC25 = 10_6m), while ZK 62711 had no effect. These data show an inhibitory effect of cyclic AMP on histamine release to be involved with basophils, whereas cyclic GMP is predominantly involved with mast cells. It is suggested that the antianaphylactic properties of cyclic nucleotide phosphodiesterase inhibitors are mainly linked to the increase of cyclic GMP.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Effects of Cyclic Amp‐ and Cyclic Gmp‐phosphodiesterase Inhibitors on Immunological Release of Histamine and on Lung Contraction

Frossard¹,

Landry²,

Pauli³

et al. 1981

British J Pharmacology

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“…We have yet to evaluate fully the contribution of possible alternative mechanisms. It appears, for example, unlikely that the effect of the drugs is due to inhibition (Coulson et al, 1977) of phosphodiesterase, as theophylline did not alter McC3-I growth. Theophylline has in fact been found to exert anti-tumour effects in some systems (Webb et al, 1972) but even these may result from prostaglandin antagonism (Manku & Horrobin, 1976).…”

Section: Effect Of Tumour-and Indomethacin On Antibody Synthesismentioning

confidence: 99%

Mechanism of inhibition of tumour growth by aspirin and indomethacin

Lynch¹,

Castes²,

Astoin³

et al. 1978

Br J Cancer

161

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Summary.-The growth of a 3-methylcholanthrene-induced fibrosarcoma of C3H mice was inhibited by aspirin and indomethacin. While the tumour contained relatively high concentrations of PGE2-like material, that were markedly diminished by indomethacin treatment, our results did not confirm the recently proposed hypothesis that the anti-tumour effect arises from a restoration of depressed immune function. For example, mice that had completely eliminated their tumours under indomethacin administration were not immune to rechallenge. The tumour-bearing animals were not non-specifically immunodepressed, as their splenic PFC responses against SRBC were enhanced. However, while indomethacin augmented the PFC response in normal mice, this adjuvant effect was depressed in tumour-bearing animals. The spleen-cell PHA responses of tumour bearers were severely depressed, and such cells suppressed the PHA response of normal cells. Only after prolonged indomethacin treatment did animals (with comparable tumour burdens) show weak PHA responses and somewhat diminished suppressive activity.Possible alternative mechanisms, such as direct cytotoxicity, or inhibition of inflammation, phosphodiesterase activity, blood coagulation or calcium availability were not implicated (nor definitively excluded) in the anti-tumour effect.

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“…Chemically, sodium nivimedone is one of a novel series of 2-nitroindane-1 ,3-diones showing antiallergic activity (Figure 1). The compound inhibited IgE-mediated passive cutaneous anaphylactic (PCA) reactions in the rat (Spicer, Ross & Smith, 1975) and the antigen-induced release of histamine from human lung passively sensitized with atopic serum (Coulson, Ford, Marshall, Walker, Wooldridge, Bowden & Coombs, 1977). The pharmacological potency of sodium nivimedone when compared to DSCG was 42 times greater in the human lung system and approximately ten times greater in rat PCA (Coulson et al, 1977).…”

Section: Introductionmentioning

confidence: 99%

“…The compound inhibited IgE-mediated passive cutaneous anaphylactic (PCA) reactions in the rat (Spicer, Ross & Smith, 1975) and the antigen-induced release of histamine from human lung passively sensitized with atopic serum (Coulson, Ford, Marshall, Walker, Wooldridge, Bowden & Coombs, 1977). The pharmacological potency of sodium nivimedone when compared to DSCG was 42 times greater in the human lung system and approximately ten times greater in rat PCA (Coulson et al, 1977). In addition, single doses of sodium nivimedone given by mouth inhibited antigeninduced bronchoconstriction in man (Pauwels, Lamont & Van der Straeten, 1976).…”

Section: Introductionmentioning

confidence: 99%

The orally administered anti‐allergic agent, sodium nivimedone (BRL 10833); efficacy in bronchial asthma and effects on IgE, complement and eosinophils.

Lumb¹,

McHardy²,

Kay³

1979

Brit J Clinical Pharma

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1 Sodium nivimedone (BRL 10833) which acts similarly to disodium cromoglycate (DSCG), given at an oral dose of 200 mg thrice daily, was compared, after a preliminary standardization week, with placebo in a 6-week double-blind cross-over trial. Twenty-four non-smoking, atopic, asthmatic outpatients aged between 16 and 32 years, who were not taking corticosteroids took part. Subjects recorded symptoms and bronchodilator use each day and measured peak expiratory flow rate (PEFR) thrice daily. 2 Data was analysed separately for the twelve subjects who received placebo followed by sodium nivimedone (Group I) and those who took the treatments in the reverse order (Group II). 3 In Group I subjects, with sodium nivimedone, bronchodilator use decreased, symptom scores improved and there was a significant improvement in overall PEFR as well as the separated morning and evening values. When symptom scores were expressed as a percentage of the placebo disability index, wheezing, chest tightness, cough and asthma on activity showed significant improvement. 4 Subjects in Group II showed no improvement in any of these variables when drug was compared to placebo. 5Sodium nivimedone did not appear to have any effect on circulating eosinophil levels, and concentrations of serum IgE, C3 and C4. 6 There was no clinical or laboratory evidence that sodium nivimedone had any untoward effect in the doses given. 7 Sodium nivimedone appeared to be of benefit in the subjects studied. The importance of appreciating the order of treatments and the value of frequent serial objective and subjective measures of disability backed up by appropriate data processing is stressed.

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Interrelationship of cyclic nucleotides and anaphylactic reactions

Cited by 40 publications

References 25 publications

Effects of Cyclic Amp‐ and Cyclic Gmp‐phosphodiesterase Inhibitors on Immunological Release of Histamine and on Lung Contraction

Effects of Cyclic Amp‐ and Cyclic Gmp‐phosphodiesterase Inhibitors on Immunological Release of Histamine and on Lung Contraction

Mechanism of inhibition of tumour growth by aspirin and indomethacin

The orally administered anti‐allergic agent, sodium nivimedone (BRL 10833); efficacy in bronchial asthma and effects on IgE, complement and eosinophils.

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