Specific receptors for prostaglandins in airways

Gardiner, P.J.; Collier, H. O. J.

doi:10.1016/0090-6980(80)90116-1

Cited by 106 publications

(54 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The extent to which blockade of contractions is due to interaction with various prostanoid receptors is therefore not known, but it seems likely that rat gastric fundus contains a multiplicity of prostanoid receptor types. Other authors have reached this conclusion with regard to lung tissue (Gardiner & Collier, 1980 …”

Section: Discussionmentioning

confidence: 68%

Antagonism of Prostanoid‐induced Contractions of Rat Gastric Fundus Muscle by Sc‐19220, Sodium Meclofenamate, Indomethacin or Trimethoquinol

Bennett

Jarosik

Sanger

et al. 1980

British J Pharmacology

View full text Add to dashboard Cite

3 The effect of the cyclo-oxygenase inhibitor sodium meclofenamate, 1 or 2 1tg/ml, on 6,15-diketo-PGFl, or thromboxane B2 was similar to the small antagonism of ACh, whereas the other prostanoids were blocked to greater extents. Indomethacin, 1 jig/ml, also reduced contractions to the prostanoids, but antagonism of the PGH2 epoxymethano analogues was considerably less than with meclofenamate. 4 The ,B-adrenoceptor stimulant trimethoquinol, 50 ng/ml, was the most potent prostanoid antagonist tested; all the prostanoids except PGE2 were antagonized more than ACh.

show abstract

Section: Discussionmentioning

confidence: 68%

Antagonism of Prostanoid‐induced Contractions of Rat Gastric Fundus Muscle by Sc‐19220, Sodium Meclofenamate, Indomethacin or Trimethoquinol

Bennett

Jarosik

Sanger

et al. 1980

British J Pharmacology

View full text Add to dashboard Cite

show abstract

“…PGI2 is produced spontaneously in low concentration from human airway and lung parenchymal tissue under normal conditions with an increase occurring after antigen challenge (Schulman et al, 1982). PGI2 has been shown to relax human bronchial muscle (Gardiner & Collier, 1980) and it has been proposed that it may play a role in regulation of airway diameter (Schulman et al, 1982). PGI2 has also been demonstrated to be an antichemotactic agent (Weissmann et al, 1980).…”

Section: Plasma Txb2mentioning

confidence: 99%

Lung function and plasma levels of thromboxane B2, 6‐ketoprostaglandin F1 alpha and beta‐thromboglobulin in antigen‐induced asthma before and after indomethacin pretreatment.

Shephard¹,

Malan²,

Macfarlane³

et al. 1985

Brit J Clinical Pharma

View full text Add to dashboard Cite

1 The effect of specific antigen challenge on the lung function of eight allergic asthmatic patients after placebo and indomethacin pretreatment has been investigated. 2 Plasma levels of thromboxane B2(TxB2), metabolite of thromboxane A2, 6-ketoPGFia, metabolite of epoprostenol, (prostacyclin, PGI2) and ,-thromboglobulin (,TBG) following antigen challenge in these eight patients have also been measured after placebo and indomethacin pretreatment. 3 Each patient underwent two antigen inhalations 1 week apart. One challenge took place after 4 days pretreatment with indomethacin capsules 25 mg four times daily, and the other took place following 4 days placebo pretreatment, one matched capsule four times daily. The order of administration was random but balanced and blind with respect to the patient. 4 Following placebo pretreatment two patients presented with an early antigen response only, four presented with a biphasic antigen response and two presented with a delayed antigen response only. The asthmatic response for each patient was consistent on reexposure. 5 Indomethacin pretreatment suppressed the delayed antigen induced asthmatic response. This suppression was reproducible. 6 There was a rise in plasma TxB2 levels on antigen challenge following placebo pretreatment but not following indomethacin pretreatment, whereas there was a rise in 6-keto-PGF1I after antigen challenge following indomethacin but not placebo pretreatment.7 No significant change in plasma ,BTBG or platelet counts from control values was observed following antigen challenge with either placebo or indomethacin pretreatment. 8 It is suggested that the production of PGI2 and suppression of TxA2 by indomethacin pretreatment contribute to the suppression of the delayed antigen induced asthmatic response and that platelets play a minimal role in this process.Keywords thromboxane B2 6-keto-prostaglandin Fla P-thromboglobulin platelets indomethacin antigen-induced asthma

show abstract

“…Several investigators have demonstrated that, in guinea-pig trachea (presumably with the epithelium intact), exogenous arachidonic acid causes relaxation associated with an elevated release of prostaglandin E2 (PGE2) (Burka et al, 1981;Spannhake et al, 1981). In addition, low concentrations ofPGE2 are often excitatory in guineapig trachea (Gardiner & Collier, 1980 Arachidonate, either at a single, high concentration, )r the effect of or cumulatively added, elicited contractions in isolated traindomethacin-treated trachea irrespective of whether (1 JM) plus or not the epithelium was present. Previous studies i), and epith- (Burka, 1985;Mansour & Daniel, 1986) also showed controls; (0) that indomethacin converts arachidonic acid-induced trachea; (U) tracheal relaxation into contraction.…”

Section: Effect Of Indomethacin Be Utilized Inmentioning

confidence: 99%

Relaxation of guinea‐pig tracheal smooth muscle to arachidonate is converted to contraction following epithelium removal

Farmer

Hay²,

Raeburn³

et al. 1987

British J Pharmacology

View full text Add to dashboard Cite

The effect of epithelium removal on responses of guinea‐pig isolated trachealis to sodium arachidonate has been examined. Arachidonate (100 μm) caused relaxation of epithelium‐intact preparations, but following epithelium removal, the response to arachidonate was converted to contraction. In the presence of indomethacin (1 μm), arachidonate caused contraction in intact and denuded trachea. Arachidonate also produced concentration‐dependent effects, the qualitative nature of which varied with the presence or absence of the epithelium. In the presence of indomethacin, tracheal strips contracted in a concentration‐dependent manner whether or not the epithelium had been removed. Nordihydroguaiaretic acid (NDGA; 11 μm) markedly inhibited the contractile response of denuded strips to arachidonate. In intact tissues this lipoxygenase inhibitor converted the arachidonate‐induced relaxation to a concentration‐dependent contraction. The contraction to arachidonate, in the presence of NDGA, was epithelium‐dependent. In the presence of both indomethacin and NDGA, responses to arachidonate were abolished. It is concluded that the relaxation of guinea‐pig trachea to arachidonic acid is epithelium‐dependent and is mediated by an inhibitory product of the cyclo‐oxygenase metabolic pathway. The contraction in denuded trachea, and trachea in the presence of indomethacin, may be mediated by lipoxygenase products of arachidonic acid metabolism, i.e. peptidoleukotrienes. The mediator of the epithelium‐dependent contraction in NDGA‐treated tissues is unknown.

show abstract

Specific receptors for prostaglandins in airways

Cited by 106 publications

References 25 publications

Antagonism of Prostanoid‐induced Contractions of Rat Gastric Fundus Muscle by Sc‐19220, Sodium Meclofenamate, Indomethacin or Trimethoquinol

Antagonism of Prostanoid‐induced Contractions of Rat Gastric Fundus Muscle by Sc‐19220, Sodium Meclofenamate, Indomethacin or Trimethoquinol

Lung function and plasma levels of thromboxane B2, 6‐ketoprostaglandin F1 alpha and beta‐thromboglobulin in antigen‐induced asthma before and after indomethacin pretreatment.

Relaxation of guinea‐pig tracheal smooth muscle to arachidonate is converted to contraction following epithelium removal

Contact Info

Product

Resources

About