THE EFFECT OF PGE<sub>1</sub> ON CYCLIC AMP AND ION MOVEMENTS IN TURKEY ERYTHROCYTES

Shaw, Jane E.; Gibson, WR; Jessup, Sheila J.; Ramwell, Peter W.

doi:10.1111/j.1749-6632.1971.tb53195.x

Cited by 42 publications

(10 citation statements)

References 25 publications

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“…When increasing concentrations of isoproterenol were tested for the effect on uterine cAMP accumulation in the presence or absence of 2 ,uM PGE2, inhibition was first noted when a potent stimulatory concentration of isoproterenol was used, suggesting a relation between the PGE2 inhibitory site and the ,3-adrenergic receptor. These results are consistent with those of Marumo and Edelman (14) and of Shaw et al (15), indicating that the inhibition of hormone effects produced by prostaglandins was associated with a decrease of tissue cAMP.…”

Section: Methodssupporting

confidence: 83%

Hormonal Interactions in the Uterus: Inhibition of Isoproterenol-Induced Accumulation of Adenosine 3′:5′-Cyclic Monophosphate by Oxytocin and Prostaglandins

Bhalla

Sanborn

Korenman

1972

Proc. Natl. Acad. Sci. U.S.A.

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Interactions of hormones stimulating and inhibiting uterine contraction were studied in vitro in uteri from oophorectomized rats. The ,3-adrenergic effector, isoproterenol, a potent inhibitor of contraction, produced a dose-related increase of adenylate cyclase and accumulation of adenosine 3' :5'-cyclic monophosphate (cAMP) that was inhibitable by propranolol. Oxytocin, which stimulates contraction, effectively inhibited accumulation of uterine cAMP induced by isoproterenol in the presence or absence of theophylline. Prostaglandins E2 and F2a, each at a maximum effective concentration of 0.5 AMM, also inhibited accumulation of cAMP induced by isoproterenol, consistent with their effect in stimulation of uterine contraction. Prostaglandin E2, but not prostaglandin F2a, stimulated cAMP accumulation in a dose-related manner at concentrations in excess of 0.5 MM. Neither propranolol nor oxytocin inhibited that response. Bovine endometrial adenylate cyclase failed to respond to isoproterenol but was stimulated by prostaglandins El and E2. When myometrial preparations were studied, isoproterenol stimulation and prostaglandin effects were observed as for whole castrate uterus. The competitive physiological actions of ,B-adrenergic effectors on the one hand, and oxytocin and prostaglandins on the other hand, are based on their influences on a myometrial adenylate cyclase. Stimulation of uterine cAMP accumulation by prostaglandin Ea is due to action at a different and unrelated site.Uterine tissue is designed to respond specifically to hormonal influences in order to provide the appropriate environment for implantation, fetal growth and development, and parturition. It appears to be ideal for study of the relationship between steroid-mediated and cAMP-mediated responses. Recently, it was shown that smooth muscle, particularly uterus, has an adenylate cyclase system whose activation by ,B-adrenergic effectors resulted in inhibition of contractility (1-4). It was further demonstrated that contractions produced by oxytocin, acetylcholine, and calcium were inhibited by fl-adrenergic effectors, theophylline, and dibutyryl-cAMP (3, 4) in association with an increase in adenylate cyclase activity (5-7). Prostaglandins, particularly those of the E series, are potent stimulators of uterine contraction despite the fact that they stimulate uterine adenylate cyclase activity (7,8).In these studies, we show that the stimulatory effects of oxytocin and prostaglandins E2

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Section: Methodssupporting

confidence: 83%

Hormonal Interactions in the Uterus: Inhibition of Isoproterenol-Induced Accumulation of Adenosine 3′:5′-Cyclic Monophosphate by Oxytocin and Prostaglandins

Bhalla

Sanborn

Korenman

1972

Proc. Natl. Acad. Sci. U.S.A.

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“…Indomethacin significantly increased pentagastrin-stimulated secretion, which is compatible with a negative feed-back inhibitory role of prostaglandins in the mucosa, operative during stimulated secretion. An increase in basal and pentagastrin-stimulated secretion has been observed in pylorus-ligated rats, following chronic administration of 5, 8, 11, 14-eicosa tetraynoic acid (Shaw, Jessup & Ramwell, 1972) which inhibits prostaglandin synthesis. In contrast, indomethacin failed to augment pentagastrin-or histamine-stimulated acid secretion in man (Winship & Bernard, 1970;Bennett, Stamford & Unger, 1973) and decreased secretion in the dog (Nicoloff, 1968 (Chvasta & Cooke, 1972), and may have masked significant changes in acid secretion in dog and man.…”

Section: Discussionmentioning

confidence: 99%

Investigation of the Vasodilator and Antisecretory Role of Prostaglandins in the Rat Gastric Mucosa by Use of Non‐steroidal Anti‐inflammatory Drugs

Main

Whittle

1975

British J Pharmacology

171

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The effects of non‐steroidal anti‐inflammatory drugs on gastric acid secretion and mucosal blood flow were studied in the rat. Indomethacin, in ulcerogenic doses, caused a dose‐dependent rise in pentagastrin‐stimulated acid secretion, but decreased mucosal blood flow per unit acid secretion. During resting conditions, indomethacin had no significant effect on acid output, but reduced mucosal blood flow. Pretreatment with indomethacin, phenylbutazone or meclofenamate potentiated the secretory response to dibutyryl cyclic adenosine 3′,5′‐monophosphate. Indomethacin markedly reduced the mucosal prostaglandin‐like activity at a time when mucosal erosion formation had reached steady levels. These results provide evidence that prostaglandins have a local role in the regulation of blood flow and acid secretion in the rat gastric mucosa, and suggest that non‐steroidal anti‐inflammatory drugs cause mucosal erosions by disrupting these processes.

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“…Heretofore this system had been found to exhibit significant enzyme activity only upon addition of 3-adrenergic agonists or fluoride (12)(13)(14)(15). Cholera toxin, if added to intact erythrocytes, increases adenylate cyclase activity and alters the kinetics of the enzyme's interactions with both epinephrine and fluoride.…”

mentioning

confidence: 99%

Mode of Action of Cholera Toxin: Stabilization of Catecholamine-Sensitive Adenylate Cyclase in Turkey Erythrocytes

Field

1974

Proc. Natl. Acad. Sci. U.S.A.

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Preincubating turkey erythrocytes with cholera toxin alters their adenylate cyclase (EC 4.6.1.1) system: basal activity, maximal epinephrine-stimulatable activity, and affinity of the enzyme reaction for epinephrine are all increased. Pretreatment of erythrocytes with choleragenoid prevents these changes. Cholera toxin does not alter [PHlepinephrine uptake by intact erythrocytes. The increase in epinephrine-stimulatable cyclase activity appears to occur at the expense of fluoridestimulatable activity, which is decreased by the toxin. In lysates from both toxin-treated and control cells, maximally stimulating amounts of epinephrine and fluoride, when added in combination, have a nearly additive effect on cyclase activity. These observations suggest that the adenylate cyclase system of the turkey erythrocyte may exist in two interconvertible forms, one that is catecholamine-responsive but fluoride-insensitive, and another that is fluoride-sensitive but not coupled to catecholamine receptors. Cholera toxin appears to stabilize the enzyme in its hormone receptor-coupled form.

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THE EFFECT OF PGE₁ ON CYCLIC AMP AND ION MOVEMENTS IN TURKEY ERYTHROCYTES

Cited by 42 publications

References 25 publications

Hormonal Interactions in the Uterus: Inhibition of Isoproterenol-Induced Accumulation of Adenosine 3′:5′-Cyclic Monophosphate by Oxytocin and Prostaglandins

Hormonal Interactions in the Uterus: Inhibition of Isoproterenol-Induced Accumulation of Adenosine 3′:5′-Cyclic Monophosphate by Oxytocin and Prostaglandins

Investigation of the Vasodilator and Antisecretory Role of Prostaglandins in the Rat Gastric Mucosa by Use of Non‐steroidal Anti‐inflammatory Drugs

Mode of Action of Cholera Toxin: Stabilization of Catecholamine-Sensitive Adenylate Cyclase in Turkey Erythrocytes

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THE EFFECT OF PGE1 ON CYCLIC AMP AND ION MOVEMENTS IN TURKEY ERYTHROCYTES

Cited by 42 publications

References 25 publications

Hormonal Interactions in the Uterus: Inhibition of Isoproterenol-Induced Accumulation of Adenosine 3′:5′-Cyclic Monophosphate by Oxytocin and Prostaglandins

Hormonal Interactions in the Uterus: Inhibition of Isoproterenol-Induced Accumulation of Adenosine 3′:5′-Cyclic Monophosphate by Oxytocin and Prostaglandins

Investigation of the Vasodilator and Antisecretory Role of Prostaglandins in the Rat Gastric Mucosa by Use of Non‐steroidal Anti‐inflammatory Drugs

Mode of Action of Cholera Toxin: Stabilization of Catecholamine-Sensitive Adenylate Cyclase in Turkey Erythrocytes

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THE EFFECT OF PGE₁ ON CYCLIC AMP AND ION MOVEMENTS IN TURKEY ERYTHROCYTES