Prostaglandins

Ramwell, Peter W.; Shaw, Jane E.; Clarke, Gregory B.; Grostic, M.F.; Kaiser, D.; Pike, J. E.

doi:10.1016/0079-6832(71)90029-2

Cited by 35 publications

(18 citation statements)

References 118 publications

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“…This is supported by the finding that PGF 2a does reduce ovarian venous blood flow in the rat and rabbit 350 SPEROFF AND RAMWELL Volume 30 (19). Since only PGF 2a is a potent venoconstrictor [the other prostaglandins are potent vasodilating and hypotensive agents (20)], this would also explain the luteolytic ineffectiveness of the other prostaglandins when given in vivo.…”

Section: Discussionmentioning

confidence: 99%

Prostaglandin Stimulation ofin VitroProgesterone Synthesis

Speroff¹,

Ramwell²

1970

The Journal of Clinical Endocrinology & Metabolism

179

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Bovine corpora lutea slices were incubated with prostaglandins and gonadotropins. All the prostaglandins tested (PGE 2 , PGE X , PGFjo and PGAi) were found to be steroidogenic, stimulating both the production of progesterone as measured in micrograms and the incorporation of radioactivity from acetate-l-u C. Prostaglandin E2 (PGE 2 ) gave the greatest effect, being approximately half as effective as luteinizing hormone (LH) on a molar basis. There were similarities between gonadotropin and prostaglandin. Cycloheximide (1 HIM) equally blocked the steroidogenic response to both PGE 2 and LH, the specific activities of the progesterone formed in the presence of prostaglandins and that formed in the presence of gonadotropins were approximately of the same order of magnitude, the time-response curves of PGE 2 and LH were similar, and there was no additive effect when prostaglandins were added to luteal slices incubated with saturating doses of either LH or human chorionic gonadotropin (HCG). These results are in contrast to the in vivo luteolytic effect of PGF 2 Q , and it is unlikely, therefore, that the luteolytic effect of PGF 2a is due to a direct inhibition of luteal steroidogenesis. Thus, the in vitro and in vivo effects of prostaglandins may represent 2 different mechanisms of action. (J Clin Endocr 30: 345, 1970)

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Section: Discussionmentioning

confidence: 99%

Prostaglandin Stimulation ofin VitroProgesterone Synthesis

Speroff¹,

Ramwell²

1970

The Journal of Clinical Endocrinology & Metabolism

179

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“…Certain fatty acids that are not precursors to prostaglandins have been shown to inhibit their biosynthesis (Pace-Asciak and Wolfe, 1968 ;Nugteren, 1970). Prostaglandins are widespread in occurrence in mammalian tissues and possess diverse physiological activ- ities Ramwell et al, 1968;Horton, 1969). Recently two new prostaglandin derivatives were isolated from marine invertebrates (Weinheimer and Spraggins, 1969).…”

mentioning

confidence: 99%

Novel prostaglandin derivative formed from arachidonic acid by rat stomach homogenates

Pace-Asciak¹,

Wolfe²

1971

Biochemistry

160

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pseudouridine was prepared using the ribonuclease-catalyzed reaction described by Heppel et al. (1955). Cytidine 2',3'cyclic phosphate (0.1 mmole) and pseudouridine (100 mg) were dissolved in 0.015 M Tris-chloride buffer (pH 7; 5 ml) and treated with pancreatic ribonuclease (0.1 mg) at 37" for 75 min. The mixture was then shaken with isoamyl alcohol (0.6 ml) and chloroform (0.15 ml) and streaked on Whatman No. 3MM chromatographic paper (66 cm). The components of the mixture were separated with solvent system B and the dinucleoside phosphate band was cut out and eluted (yield, 30 ODU). This product was found to be completely degradable by ribonuclease to cytidine 3'-phosphate and pseudouridine. The dinucleoside phosphate (20 ODU) was dissolved in 0.05 M sodium borate buffer (pH 8.5 ; 0.3 ml) and treated with Cmcp-toluenesulfonate (40 mg). The mixture was allowed to stand for 20 hr. At this time paper chromatography in solvent systems A and B showed that about 70% of the material had been converted to Cmc derivatives. The dinucleoside phosphate and its mono-Cmc derivative had RF values 0.41 and 0.61 (solvent system A); 0.18 and 0.26 (solvent system B), respectively. The mixture was treated with concentrated ammonia for 2 hr and then applied to Whatman No. 3MM chromatographic paper and then separated in solvent system B. The Cmc-dinucleoside phosphate (6 ODU) was dissolved in 0.02 M sodium phosphate buffer (pH 7.0; 0.2 ml) and treated with pancreatic ribonuclease (2.5 pg) at 37" for 4 hr. Paper chromatography in solvent system A showed that about 70% of the Cmc derivative had been converted into a mixture of cytidine 3'-phosphate and Cmc-pseudouridine. With twice the amount of enzyme under the same conditions it was possible to hydrolyze all the dinucleoside phosphate to its components.

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“…In general, prostaglandins (PG's) ' appear to be ubiquitous and have been demonstrated to modulate a variety of tissue and hormone system effects (1 (2). Since the adrenergic nervous system has profound regulatory effects upon insulin secretion (3,4) In all of the studies to be described, intravenous glucose was injected as a 2-g pulse (4 ml of a 50% glucose solution) in less than 3 s. Unless otherwise indicated, all infusions other than the glucose injections were given through a catheter placed in the femoral vein opposite to the one used for sample collection.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of In Vivo Insulin Secretion by Prostaglandin E1

Robertson¹,

Dj²,

Porte³

et al. 1974

J. Clin. Invest.

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A B S T R A C T To determine the effect of prostaglandin E1 (PGE1) infusion upon in vivo insulin secretion, serum insulin responses after an intravenous glucose pulse (2 g) were measured before and during an intravenous infusion of PGE1 (10 Ag/min) in 11 anesthetized dogs. Circulating insulin decreased significantly during PGE1 infusion, and insulin responses after glucose during PGE1 infusion were significantly less than control responses. Three dogs received PGE1 infusions into the thoracic aorta to preclude pulmonic and hepatic degradation of PGE1 before its arrival at the pancreatic artery; inhibition of insulin secretion was again seen. Inhibition of insulin secretion could not be related to the degree of arterial hypotension induced by intravenous PGE1, and despite alpha adrenergic blockade with intravenous phentolamine, PGEi-induced inhibition of glucose-stimulated insulin responses persisted. Significant increments in systemically circulating PGE levels during intravenous PGE1 infusions were documented by radioimmunoassay. These studies demonstrate that systemic PGE1 infusion inhibits insulin secretion and that this effect could not be shown to be dependent upon alpha adrenergic activity.

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Prostaglandins

Cited by 35 publications

References 118 publications

Prostaglandin Stimulation ofin VitroProgesterone Synthesis

Prostaglandin Stimulation ofin VitroProgesterone Synthesis

Novel prostaglandin derivative formed from arachidonic acid by rat stomach homogenates

Inhibition of In Vivo Insulin Secretion by Prostaglandin E1

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