Pertussis and cholera toxins inhibit prostaglandin synthesis in rat astrocyte cultures at distinct metabolic steps

1991 ◽  
Vol 42 (6) ◽  
pp. 1267-1271 ◽  
Author(s):  
Peter J. Gebicke-Haerter ◽  
Angelika Schobert ◽  
Georg Hertting
Keyword(s):  
Prostaglandin Synthesis ◽  
Inhibit Prostaglandin Synthesis ◽  
Rat Astrocyte

Liposome-mediated augmentation of antioxidant defenses in fetal rat pneumocytes

1990 ◽  
Vol 258 (4) ◽  
pp. L165-L172 ◽  
Author(s):  
A. K. Tanswell ◽  
D. M. Olson ◽  
B. A. Freeman
Keyword(s):  
Dna Synthesis ◽  
Prostaglandin Synthesis ◽  
Antioxidant Defenses ◽  
Fetal Cells ◽  
Mediated Effects ◽  
Lactate Dehydrogenase Release ◽  
Low Concentrations ◽  
Inhibit Prostaglandin Synthesis ◽  
Fetal Rat ◽  
Endogenous Antioxidant

Cultured pneumocytes, prepared from fetal rat lung, are growth inhibited and have increased lactate dehydrogenase release and prostaglandin synthesis in response to 50 and 95% O2 exposure. The uptake of cationic liposomes by these fetal cells is more rapid and extensive than is the case with cultured adult pneumocytes. Protection of fetal pneumocytes against the cytotoxic effects of 50 or 95% O2 by liposome-entrapped antioxidant enzymes requires a liposome phospholipid concentration of only 1 nmol/cm2, compared with 45 nmol/cm2 for adult cells, which is a cytotoxic phospholipid concentration for the fetal cells. Despite this capacity of low concentrations of liposomes containing superoxide dismutase and catalase to increase endogenous antioxidant enzyme content, and to protect against cell death, such treatment does not attenuate O2-mediated alterations of cell growth or prostaglandin release. Inhibition of pneumocyte DNA synthesis, by elevated O2 concentrations, cannot be attributed to an autocrine effect of enhanced prostaglandin synthesis, because the addition of 50 microM ibuprofen to inhibit prostaglandin synthesis does not prevent O2-mediated effects on DNA synthesis.

The Effects of Meclofenamate, Captopril and Phentolamine on Organ Blood Flow in the Conscious Rabbit

1981 ◽  
Vol 61 (1) ◽  
pp. 97-105 ◽  
Author(s):  
R. A. Banks ◽  
L. J. Beilin
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Hepatic Artery ◽  
Peripheral Resistance ◽  
Prostaglandin Synthesis ◽  
Organ Blood Flow ◽  
Inhibit Prostaglandin Synthesis ◽  
Conscious Rabbits ◽  
Artery Flow ◽  
Intravenous Sodium

1. Systemic and regional vascular changes were measured in conscious rabbits after intravenous sodium meclofenamate, captopril and phentolamine. These drugs were used respectively to inhibit prostaglandin synthesis and angiotensin-converting enzyme, and to block α-adrenoceptors. 2. Meclofenamate reduced renal and adrenal blood flow by 11 and 28% respectively, and doubled hepatic artery flow. The effect on renal and adrenal flow persisted in the presence of phentolamine. 3. Captopril decreased estimated peripheral resistance and increased cardiac output without changing arterial pressure. Kidney and adrenal flow increased by 70 and 21% respectively. 4. Phentolamine reduced arterial pressure and doubled flow to skeletal muscle and increased hepatic artery flow to the liver. 5. Splenic blood flow was unaffected by meclofenamate, captopril or phentolamine alone. Meclofenamate given after captopril caused a halving of splenic flow and a rise in arterial pressure; these effects were prevented by phentolamine. 6. The results point to a continuing effect of prostaglandin synthesis in maintaining blood flow to the kidney and adrenal gland independent of α-adrenoceptor activation in resting conscious rabbits. An important modulating effect of prostaglandins on sympathetic vascular tone in the spleen is suggested.

scholarly journals Renal effects of drugs that inhibit prostaglandin synthesis

1980 ◽  
Vol 18 (5) ◽  
pp. 609-622 ◽  
Author(s):  
Michael J. Dunn ◽  
Edward J. Zambraski
Keyword(s):  
Prostaglandin Synthesis ◽  
Renal Effects ◽  
Inhibit Prostaglandin Synthesis

scholarly journals Many Putative Endocrine Disruptors Inhibit Prostaglandin Synthesis

2011 ◽  
Vol 119 (4) ◽  
pp. 534-541 ◽  
Author(s):  
David M. Kristensen ◽  
Maria L. Skalkam ◽  
Karine Audouze ◽  
Laurianne Lesné ◽  
Christele Desdoits-Lethimonier ◽  
...  
Keyword(s):  
Endocrine Disruptors ◽  
Prostaglandin Synthesis ◽  
Inhibit Prostaglandin Synthesis

Furosemide action on collecting ducts: effect of prostaglandin synthesis inhibition

1983 ◽  
Vol 244 (6) ◽  
pp. F666-F673 ◽  
Author(s):  
D. R. Wilson ◽  
U. Honrath ◽  
H. Sonnenberg
Keyword(s):  
Collecting Duct ◽  
Prostaglandin Synthesis ◽  
Water Reabsorption ◽  
Inner Medullary Collecting Duct ◽  
Nephron Segments ◽  
Inhibit Prostaglandin Synthesis ◽  
Collecting Ducts ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Medullary Collecting Duct ◽  
Furosemide Administration

The effect of furosemide on inner medullary collecting duct chloride reabsorption has not been determined, and the blunting of furosemide action by drugs that inhibit prostaglandin synthesis, while known to occur, has not been examined in detail. The effect of indomethacin and meclofenamate on furosemide diuresis was studied in the rat using clearance and collecting duct microcatheterization methods. Furosemide-treated control animals showed complete inhibition of chloride, sodium, and water reabsorption in the inner medullary collecting duct. Rats given indomethacin or meclofenamate before and during furosemide administration showed marked reduction of the chloriuresis, natriuresis, and diuresis. Reduced delivery of sodium and chloride to the beginning of the inner medullary collecting duct, associated with a decrease in glomerular filtration rate and increased reabsorption in more proximal nephron segments, was largely responsible for the reduced natriuresis and chloriuresis during inhibition of prostaglandin synthesis. In addition, indomethacin increased collecting duct NaCl reabsorption toward normal, but meclofenamate showed no such effect. The results indicate that furosemide inhibits medullary collecting duct reabsorption of chloride, sodium, and water in the rat. The blunting of diuretic action seen with inhibition of prostaglandin synthesis is largely, although not entirely, due to effects of indomethacin and meclofenamate on furosemide action at nephron sites proximal to the collecting duct.

Possible association of schizophrenia with a disturbance in prostaglandin metabolism: a physiological hypothesis

1976 ◽  
Vol 6 (3) ◽  
pp. 359-369 ◽  
Author(s):  
W. Feldberg
Keyword(s):  
Lipid A ◽  
Prostaglandin Synthesis ◽  
Prostaglandin E ◽  
Cerebral Ventricles ◽  
Prostaglandin Metabolism ◽  
Prostaglandin Level ◽  
Inhibit Prostaglandin Synthesis ◽  
Febrile Episodes ◽  
The Brain

SynopsisSchizophrenia may be associated with increased prostaglandin synthesis in certain parts of the brain. This hypothesis is based on the following findings: (1) Catalepsy, which is the nearest equivalent in animals to human catatonia, develops in cats when prostaglandin E1 is injected into the cerebral ventricles and when during endotoxin or lipid A fever the prostaglandin E2 level in cisternal c.s.f. rises to high levels; however, when fever and prostaglandin level are brought down by non-steroid anti-pyretics which inhibit prostaglandin synthesis, catalepsy disappears as well. (2) Febrile episodes are a genuine syndrome of schizophrenia.

Naproxen (naprosyn) and ketoprofen (orudis)

1974 ◽  
Vol 12 (7) ◽  
pp. 25-27
Keyword(s):  
Prostaglandin Synthesis ◽  
New Drugs ◽  
Inflammatory Activity ◽  
Inhibit Prostaglandin Synthesis ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
Low Incidence ◽  
Gastric Irritation

Naproxen (Naprosyn - Syntex) and ketoprofen (Orudis - M & B) are new drugs for treating various forms of arthropathy. For both drugs the manufacturers claim good anti-inflammatory activity with a low incidence of unwanted effects, particularly gastric irritation, in comparison with other non-steroidal anti-inflammatory drugs. If these claims can be substantiated these preparations would be valuable. Like aspirin and other non-steroidal anti-inflammatory drugs they both inhibit prostaglandin synthesis. Both are chemically related to other such drugs, for example ibuprofen (Brufen - Boots).

P2-purinoceptor induced prostaglandin synthesis in primary rat astrocyte cultures

1988 ◽  
Vol 338 (6) ◽  
pp. 704-707 ◽  
Author(s):  
Peter J. Gebicke-Haerter ◽  
Siegfried Wurster ◽  
Angelika Schobert ◽  
Georg Hertting
Keyword(s):  
Prostaglandin Synthesis ◽  
Rat Astrocyte

Reversible Renal Failure Associated with Ibuprofen: Case Report and Review of the Literature

1984 ◽  
Vol 18 (1) ◽  
pp. 27-33 ◽  
Author(s):  
Therese I. Poirier
Keyword(s):  
Renal Failure ◽  
Prostaglandin Synthesis ◽  
Predisposing Factors ◽  
Analgesic Nephropathy ◽  
Probable Case ◽  
Renal Deterioration ◽  
Inhibit Prostaglandin Synthesis ◽  
Risk Patients ◽  
Inflammatory Drugs

A report of a probable case of acute, reversible renal failure and hyperkalemia, after an increase in dose of ibuprofen, is presented. Other cases of renal dysfunction associated with various nonsteroidal anti-inflammatory drugs (NSAIDs) are reviewed. The ability of NSAIDs to inhibit prostaglandin synthesis may explain the various renal consequences. Possible predisposing factors to renal deterioration include the amount of drug consumed, presence of compromised renal blood flow, underlying renal insufficiency, nephrotoxic drug combinations, and high urinary prostaglandin excretion. Generally, the renal failure with NSAIDs is acute and reversible, though analgesic nephropathy with papillary necrosis and chronic renal failure are reported. Electrolytes, blood urea nitrogen, and serum creatinine levels need to be monitored in high-risk patients with predisposing factors and for chronic, long-term use of drugs that inhibit prostaglandin synthesis.

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