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Biomedical subjects

R J Flower

Publications and source records attributed to R J Flower.

At least 217 records · Page 12Linked to original sources
PubMed1976

Partial purification of rabbit aorta contracting substance-releasing factor and inhibition of its activity by anti-inflammatory steroids.

Rabbit aorta contracting substance-releasing factor (RCS-RF) is found in perfusates from guinea pig lungs during anaphylaxis. It has been identified as a small peptide which releases arachidonic acid from lung tissue, thus generating prostaglandin endoperoxides and tbromboxanes and causing bronchocconstriction. Anti-inflammatory steroids block the release of arachidonate by RCS-RF. In this activity their relative potency is very similar to their relative anti-inflammatory potency, suggesting that the two actions may be related.

Animals↗
PubMed1976

Genetic hypertension in rats is accompanied by a defect in renal prostaglandin catabolism.

Noradrenaline releases prostaglandins in the kidney, and in rats these augment rather than reduce vasoconstriction produced by the amine. Homogenates of kidneys of New Zealand rats inbred for hypertension exhibit lower prostaglandin inactivation by 15-hydroxydehydrogenase than controls. At the same time, augmentation of noradrenaline vasoconstriction by the released prostaglandin is exaggerated. This biochemical defect could be the inherited abnormality primarily responsible for the development of hypertension in these animals.

Animals↗
PubMed1976

Arterial walls are protected against deposition of platelet thrombi by a substance (prostaglandin X) which they make from prostaglandin endoperoxides.

Prostaglandin (PG) endoperoxides (PGG2 and PGH2) contract arterial smooth muscle and cause platelet aggregation. Microsomes from pig aorta, pig mesenteric arteries, rabbit aorta and rat stomach fundus enzymically transform PG endoperoxides to an unstable product (PGX) which relaxes arterial strips and prevents platelet aggregation. Microsomes from rat stomach corpus, rat liver, rabbit lungs, rabbit spleen, rabbit brain, rabbit kidney medulla, ram seminal vesicles as well as particulate fractions of rat skin homogenates transform PG endoperoxides to PGE- and PGF- rather than to PGX-like activity. PGX differs from the products of enzymic transformation of prostaglandin endoperoxides so far identified, including PGE2, F2alpha, D2, thromboxane A2 and their metabolites. PGX is less active in contracting rat fundic strip, chick rectum, guinea pig ileum and guinea pig trachea than are PGG2 and PGH2. PGX does not contract the rat colon. PGX is unstable in aqueous solution and its antiaggregating activity disappears within 0.25 min on boiling or within 10 min at 37degrees C. As an inhibitor of human platelet aggregation induced in vitro by arachidonic acid PGX was 30 times more potent than PGE1. The enzymic formation of PGX is inhibited by 15-hydroperoxy arachidonic acid (IC50 = 0.48 mug/ml), by spontaneously oxidised arachidonic acid (IC 50 less than 100 mug/ml) and by tranylcypromine (IC50 = 160 mug/ml). We conclude that a balance between formation by arterial walls of PGX which prevents platelet aggregation and release by blood platelets of prostaglandin endoperoxides which induce aggregation is of the utmost importance for the control of thrombus formation in vessels.

Animals↗
PubMed1976

Inflammatory effects of prostaglandin D2 in rat and human skin.

1 Intradermal injection of prostaglandin (PG) D1 and D2 in the human forearm produced a long-lasting dose-related erythema. When compared with prostaglandin E1 or E2 the order of potency for erythema production was PGE1 greater than PGE2 greater than PGD2 greater than PGD1. 2 In rat skin, prostaglandin D2 but not D1 caused an increase in vascular permeability as quantitated by the Evans blue method and the 125I-albumin extravasation technique. Prostaglandin E2 was 3-5 times more potent than prostaglandin D2. 3 Prostaglandin D2 (10 ng) potentiated the increase in vascular permeability in rat skin produced by histamine, but not that produced by bradykinin. 4 Prostaglandin D2 (10, 20 and 50 ng) did not elicit oedema or hyperalgesia in the rat paw oedema test, but potentiated carrageenan-induced oedema; hyperalgesia was potentiated by doses of 100 ng and above.

Animals↗
PubMed1976

A rapid method for the estimation of prostaglandin 15-hydroxydehydrogenase activity and its application to pharmacology.

A novel double-isotope assay for prostaglandin 15-hydroxydehydrogenase (PGDH) is described. 2 The assay is simple, rapid, precise, completely specific for PGDH, and free from artefacts. The results obtained correlate well with a conventional assay. 3 The method is versatile, being applicable to estimations of enzyme activity in cell-free systems as well as perfused organs, and is well suited to the assay of PGDH inhibitors.

Alcohol Oxidoreductases↗
PubMed1975

Some characteristics of the prostaglandin synthesizing system in rabbit kidney microsomes.

The prostaglandin synthesizing system in rabbit kidney microsomes was characterised using a radiometric assay. Three prostaglandins (F2alpha, E2 and D2) were formed form (1-14C)arachidonic acid, a small amount of prostaglandin A2 was also detected but this was formed non-enzymatically. Biosynthesis was stimulated by reduced-glutathione and 1-adrenaline and was inhibited by aspirin-like drugs. The enzyme system was sensitive to small changes in pH. There were substantial differences in drug sensitivity and optimal reaction conditions between this prostaglandin synthesizing system and the one from bovine seminal vesicles.

Aldosterone↗
PubMed1975

Seminal prostaglandins in infertile men.

The concentration of prostaglandin E (PGE) was measured in the semen of 5 men of proven fertility and in 12 men of couples who were infertile but in whom no abnormality had been detected by conventional semen analysis, postcoital test of sperm motility, endometrial biopsy, and laparoscopic dye insufflation of the fallopian tubes. In the fertile men the mean PGE concentration was 52.7 +/- 9.9 mug/ml, and in infertile men the concentration was 22.1 +/- 2.76 mug/ml; the difference between the two groups was highly significant (P less than 0.001). In five of the infertile men attempts were made to raise the PGE concentration by the administration of either corn oil, which contains the prostaglandin precursor linoleic acid, or caffeine, which inhibits prostaglandin degradation; the response to both agents was insignificant.

Caffeine↗
PubMed1975

Rapid reduction of prostaglandin 15-hydroxy dehydrogenase activity in rat tissues after treatment with protein synthesis inhibitors.

1 The capacity of rat kidneys to metabolize prostaglandins is rapidly lost when de novo protein synthesis is reduced by cycloheximide and puromycin. Enzyme activity declines to about half control values 45-75 min after a single dose of cycloheximide. Prostaglandin metabolism by the lung is also diminished. 2 These inhibitors apparently act by preventing the synthesis of new prostaglandin 15-hydroxy dehydrogenase enzyme. 3 The RNA synthesis actinomycin D has no effect on metabolism. 4 It is concluded that prostaglandin dehydrogenase is a short-lived enzyme in the cell whose replacement depends upon de novo protein (but not RNA) synthesis. The implications of this finding are discussed.

Alcohol Oxidoreductases↗