Effect of acetaminophen on prostaglandin E2 and prostaglandin F2α synthesis in the renal inner medulla of rat

Zenser, Terry V.; Mattammal, Michael B.; Herman, Ceil A.; Joshi, Shobha; Davis, Bernard B.

doi:10.1016/0304-4165(78)90378-1

Cited by 29 publications

(13 citation statements)

References 28 publications

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“…As with naproxen, acetaminophen also inhibited prostaglandin synthesis and enhanced hormone-stimulated, but not basal water flow. These studies demonstrate that acetaminophen acts as a prostaglandin synthesis inhibitor in toad bladders, as has been reported in renal medullary slices (26). When, on the other hand, endogenous prostaglandin synthesis was stimulated by administration of arachidonic acid, basal water flow was unaffected, but hormone-stimulated water flow was markedly inhibited.…”

Section: Discussionsupporting

confidence: 83%

See 1 more Smart Citation

Interaction of vasopressin and prostaglandins in the toad urinary bladder.

Bisordi¹,

Schlöndorff²,

Hays³

1980

J. Clin. Invest.

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Arachidonic acid, the specific precursor of prostaglandin synthesis, increased PCE2 synthesis twofold, and significantly inhibited AVP-and DDAVP-stimulated water flow by 60 and 75%, respectively. Naproxen and acetaminophen inhibited prostaglandin synthesis and enhanced water flow in response to AVP and DDAVP (44-54%).Our findings indicate that the toad bladder produces two prostaglandins, PGE2 and TXB2, and that vasopressin does not alter their rate of synthesis. Because agents such as acetaminophen and naproxen inhibit prostaglandin synthesis and enhance vasopressin-and DDAVP-stimulated water flow, we suggest that it is the inhibitory effect of these agents on the hormoneindependent rate of prostaglandin synthesis that is responsible for their enhancement of water flow.A preliminary report of portions of this work was presented at

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Section: Discussionsupporting

confidence: 83%

“…Acetaminophen has been reported to enhance the response to AVP in toad bladder (23,24) and have antidiuretic activity in human central diabetes insipidus (25). Recently this compound has been found to inhibit prostaglandin synthesis in rat renal medullary slices (26).…”

Section: Methodsmentioning

confidence: 99%

Interaction of vasopressin and prostaglandins in the toad urinary bladder.

Bisordi¹,

Schlöndorff²,

Hays³

1980

J. Clin. Invest.

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“…(1988), it a E < , r4reduced the in vivo synthesis of prostacyclin to a E4 ._ -v v * much greater extent than in the present investigation while in another study it appeared to have an opposite effect as it inhibited platelet aggregation in vitro by a mechanism involving arachidonic acid metabolism (Dupin et al, 1988). The effects of paracetamol on renal prostaglandins in man have not been described previously, but in animals it produces reversible, dose-dependent inhibition of renal medullary prostaglandin E2 synthesis by a direct action on cyclooxygenase without prior metabolic activation (Mattammal et al, 1979;Zenser et al, 1978). Haylor (1980) reported a reduction in urine volume, sodium excretion and osmolal output in six normally hydrated female subjects following administration of 1.5 g of paracetamol, but prostaglandins were not measured and the sodium intake was not controlled.…”

Section: Urine Volume and Osmolalitymentioning

confidence: 42%

The comparative effects of paracetamol and indomethacin on renal function in healthy female volunteers.

Prescott

Mattison

Menzies

et al. 1990

Brit J Clinical Pharma

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1 Renal function was assessed in 10 healthy female volunteers during administration of placebo, paracetamol (acetaminophen) (4.0 g daily) and indomethacin (150 mg daily) for 3 days under conditions of controlled sodium and fluid intake. 2 Paracetamol and indomethacin had no significant effect on the glomerular filtration rate and effective renal plasma flow as measured by the renal clearances of inulin, creatinine and p-aminohippurate (PAH). 3 Compared with placebo, paracetamol reduced the mean urinary excretion of prostaglandin E2 by 43% on the second day and 58% on the third treatment day (P < 0.01). With indomethacin the corresponding reductions were 73 and 80%. Paracetamol and indomethacin had much less effect on the excretion of prostaglandin 6-keto Fia, and a significant decrease was observed only on the third day. 4 The decreased urinary excretion of prostaglandin E2, produced by paracetamol was associated with a reduction in sodium excretion of more than 50% (P < 0.01) and delay in the onset of diuresis following an acute water load. 5 The renal effects of paracetamol and indomethacin appear to differ. Although indomethacin reduced prostaglandin excretion more than paracetamol it had a similar effect on sodium excretion and less initial antidiuretic action. Unlike paracetamol, indomethacin also reduced basal plasma renin activity. 6 Paracetamol reduced the total body clearance of PAH and increased its plasma halflife. This effect could be attributed to inhibition of the acetylation of PAH by paracetamol. 7 In normal use paracetamol does not appear to have the adverse renal effects associated with the non-steroidal anti-inflammatory analgesics and further studies are required to establish the clinical significance of these findings.

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“…[15][16][17] Aspirin, 7 acetaminophen, 5,6 and NSAIDS 18 have each been shown to reduce formation of vasodilator prostaglandins from arachadonic acid. In the setting of volume depletion, PGI 2 and PGE 2 enhance glomerular filtration 15,19 and reduce fractional sodium reabsorption.…”

Section: Discussionmentioning

confidence: 99%

“…4 Although aspirin and acetaminophen also influence prostaglandin homeostasis, [5][6][7] prospective data on their potential hypertensive effects have been sparse and inconclusive. 8,9 A recent study of these effects in a large cohort of younger US women demonstrated an increased incidence of hypertension in users of NSAIDs and acetaminophen but not aspirin (OR 1.86 and 2.00, respectively, for the highest use category, PϽ0.001).…”

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confidence: 99%

Nonnarcotic Analgesic Use and the Risk of Hypertension in US Women

et al. 2002

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Abstract-Acetaminophen, aspirin, and other nonsteroidal anti-inflammatory drugs (NSAIDs) are widely consumed. Each is theoretically capable of elevating blood pressure by altering prostaglandin homeostasis; however, there is little prospective information on the relation between these agents and physician-diagnosed hypertension. We examined the association between the use of aspirin, acetaminophen, or NSAIDs and incident hypertension in a prospective cohort study of 51 630 women 44 to 69 years of age in 1990 who had no history of hypertension or chronic renal insufficiency. Analgesic use was assessed in 1990 by a mailed questionnaire, and the women were followed for 8 years. Key Words: hypertension, essential Ⅲ drug therapy Ⅲ blood pressure Ⅲ risk factors A spirin, acetaminophen, and ibuprofen are the three most commonly used medications among adults 18 years of age and older, according to a national survey of US households conducted between 1998 and 1999. 1 Seventeen percent of respondents reported using aspirin in the preceding week, 23% reported acetaminophen use, and 17% ibuprofen use. Prevalence of use was greater among women than men for acetaminophen and ibuprofen.Short-term prospective studies suggest nonsteroidal antiinflammatory drugs (NSAIDs) can cause acute elevations in blood pressure, 2,3 but a diagnosis of hypertension was used as the primary outcome in only one case-control study. 4 Although aspirin and acetaminophen also influence prostaglandin homeostasis, 5-7 prospective data on their potential hypertensive effects have been sparse and inconclusive. 8,9 A recent study of these effects in a large cohort of younger US women demonstrated an increased incidence of hypertension in users of NSAIDs and acetaminophen but not aspirin (OR 1.86 and 2.00, respectively, for the highest use category, PϽ0.001). 10 Twenty-four percent of US adults and 50% to 70% of those Ͼ60 years of age have hypertension. 11 Even small elevations in blood pressure caused by nonnarcotic analgesic use could affect cardiovascular morbidity and mortality. 12 To examine this issue, we studied the association between the use of aspirin, acetaminophen, and NSAIDs and incident hypertension in a large cohort of US women. Methods The Nurses' Health StudyThe Nurses' Health Study cohort was assembled in 1976 when 121 700 female registered nurses, 30 to 55 years of age, completed and returned a mailed questionnaire. 13 Follow-up questionnaires have been mailed every 2 years to update information on healthrelated behaviors and medical events. In 1990, questions were included regarding frequency of use of acetaminophen, aspirin, and other NSAIDs. Study PopulationThe 1990 questionnaire was answered by 85 625 women. Women who reported a history of hypertension (nϭ27 344) or chronic kidney failure (nϭ10) on or before the 1990 questionnaire were excluded from the study, as were women who did not answer any of the questions on analgesic use (nϭ336). We also excluded subjects who did not report having had a physical examination between 1988

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Effect of acetaminophen on prostaglandin E2 and prostaglandin F2α synthesis in the renal inner medulla of rat

Cited by 29 publications

References 28 publications

Interaction of vasopressin and prostaglandins in the toad urinary bladder.

Interaction of vasopressin and prostaglandins in the toad urinary bladder.

The comparative effects of paracetamol and indomethacin on renal function in healthy female volunteers.

Nonnarcotic Analgesic Use and the Risk of Hypertension in US Women

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