A new technique for the measurement of urinary 6-keto-prostaglandin F1α: normal values in adults

Benzoni, Daniel; Vincent, Madeleine; Cuisinaud, G.; Sassard, J

doi:10.1016/0009-8981(82)90302-3

Cited by 24 publications

(9 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Urinary 6-keto-PGFla and TxB2 were determined using published methods (Benzoni et al 1982;Geoffroy et al 1985) which include an extraction followed by separation by high performance liquid chromatography and a specific immunoassay. Urinary 11dehydro-TxB2 was measured by a specific enzymoimmunoassay which includes an extraction on Sep-Pak columns and sample purification by thin-layer chromatography (Lellouche et al 1990).…”

Section: (Ii) Analytical Methodsmentioning

confidence: 99%

BLOOD PRESSURE EFFECTS OF THROMBOXANE A₂ BLOCKADE IN SPONTANEOUSLY HYPERTENSIVE RATS

Boussairi¹,

Sacquet²,

Benzoni³

et al. 1993

Clin Exp Pharma Physio

View full text Add to dashboard Cite

1. The effects of CGS 22652, a thromboxane (Tx) A2 synthase inhibitor and TxA2/prostaglandin (PG) H2 receptor antagonist, on blood pressure (BP) were studied in conscious freely moving spontaneously hypertensive rats (SHR). 2. Three groups of 13 male SHR were subcutaneously infused from 5 to 11 weeks of age via osmotic minipumps with CGS 22652 at doses of 5 (SHRa) or 10 (SHRb) mg/kg per 24 h or with the vehicle only (SHRc). A fourth group (SHRd, n = 13) was orally treated from 3 to 11 weeks of age with CGS 22652 (30 mg/kg) given by gavage once a day. 3. CGS 22652 dose-dependently reduced the age-related increase in systolic BP. The pressor response to noradrenaline (200 ng/kg, i.v.) but not to angiotensin I or II was slightly (P < 0.05) diminished in 11 week old SHRb and SHRd compared to SHRc. Acute ganglionic blockade by trimethaphan (10 mg/kg, i.v.), as well as angiotensin converting enzyme inhibition by perindopril (2 mg/kg, i.v.) decreased BP to a similar extent in the four groups. After combined blockade of vasopressin receptors and of the autonomic nervous system and the administration of a direct vasodilator (hydralazine, 3 mg/kg, i.v.), the residual mean BP was identical in the four groups of rats. 4. Chronic treatment with CGS 22652 dose-dependent antagonized the TxA2/PGH2 receptors but did not modify the TxA2 synthesis. The urinary sodium excretion did not differ between groups. 5. In conclusion, at the doses used, CGS 22652 given either orally or subcutaneously exhibited only TxA2/PGH2 receptor blocking properties in SHR.(ABSTRACT TRUNCATED AT 250 WORDS)

show abstract

Section: (Ii) Analytical Methodsmentioning

confidence: 99%

BLOOD PRESSURE EFFECTS OF THROMBOXANE A₂ BLOCKADE IN SPONTANEOUSLY HYPERTENSIVE RATS

Boussairi¹,

Sacquet²,

Benzoni³

et al. 1993

Clin Exp Pharma Physio

View full text Add to dashboard Cite

show abstract

“…Urinary PGE2, PGF2a,, 6-keto-PGFi,, and TxB2 were determined by our previously reported methods including a high performance liquid chromatographic separation prior to sensitive radioimmunoassays (Benzoni et al, 1981(Benzoni et al, , 1982(Benzoni et al, , 1985.…”

Section: Methodsmentioning

confidence: 99%

Atrial natriuretic peptide and urinary prostaglandins in man.

Benzoni¹,

Geoffroy²,

Waeber³

et al. 1989

Brit J Clinical Pharma

View full text Add to dashboard Cite

1 In order to assess the effects of atrial natriuretic factor on the renal biosynthesis of prostaglandins (PG), the urinary excretion of PGE2, PGF20,, 6-keto-PGF10, and thromboxane (Tx)B2 were followed in eight salt-loaded healthy volunteers infused for 2 h with a non hypotensive dose of human atrial natriuretic peptide (hANP, 0.7 nmol min-1).2 Within 1 h, hANP, infusion produced a marked increase in the urinary PG output, especially of PGE2 and 6-keto-PGF10, (188 ± 21% and 202 ± 24% of the pre-infusion values respectively), followed by a significant decrease during the recovery period. 3 No correlations could be uncovered between the urinary excretion of sodium and that of any of the PGs. In contrast, during the infusion of hANP, the urinary output of PGE2 and of 6-keto-PGF10, was found positively related to the urinary flow rate (r = 0.42; P < 0.05; n = 32 and r = 0.43; P < 0.05; n = 32 respectively) as well as during the recovery period (r = 0.66, P < 0.001; n = 32 and r 0.55; P < 0.01; n = 32 respectively). 4 It was concluded that, in man, infusion of a non hypotensive dose of hANP is followed by a rise in urinary PG excretion presumably reflecting enhanced renal PG biosynthesis. This increased urinary PG excretion does not seem to be involved in the natriuretic action of hANP but might participate to its diuretic effect.

show abstract

“…Urinary concentrations of 6 keto prostaglandin Fltc (6KPGF1,) and of thromboxane B2 (TxB2) the major stable metabolites of prostacyclin and thromboxane A2 respectively, were measured by specific radioimmunoassays after a high-performance liquid chromatographic separation step (Benzoni et al, 1982;Geoffroy et al, 1985).…”

Section: Methodsmentioning

confidence: 99%

Influence of renal insufficiency on the pharmacokinetics of cicletanine and its effects on the urinary excretion of electrolytes and prostanoids.

Ferry¹,

Geoffroy²,

Pozet³

et al. 1988

Brit J Clinical Pharma

View full text Add to dashboard Cite

1 The kinetics of a single oral dose (300 mg) of cicletanine a new antihypertensive drug with diuretic properties, and its effects on the urinary excretion of electrolytes and of the major stable metabolites of prostacyclin and thromboxane A2 were studied in patients with normal renal function (n = 6), mild (n = 9) and severe (n = 10) renal insufficiency. 2 In normotensive subjects with normal renal function, cicletanine was rapidly and regularly absorbed, its apparent elimination half-life established around 7 h, and both its renal clearance (0.4 ml min-') and its cumulative renal excretion (0.85% of the administered dose), were low. Mild renal insufficiency did not significantly alter these parameters, while severe renal impairment reduced the renal clearance and the cumulative urinary excretion of cicletanine and increased its apparent elimination half-life (31 h). However the area under the plasma curve was not changed due to reduced plasma concentrations in these patients. 3 Cicletanine induced a rapid and marked (four fold as a mean) increase in the urinary excretion of water, sodium and potassium which lasted for 6 to 10 h, in subjects with normal renal function. Renal insufficiency did not alter the slope of the calculated plasma concentration-effects curves but reduced the maximum effect observed for water, sodium and potassium. 4 A single oral dose of cicletanine did not change the urinary excretion of 6-ketoprostaglandin Fla and thromboxane B2 in the three groups of patients studied, the basal values of which being found to be closely related to the creatinine clearance. 5 It was concluded that i) from a pharmacokinetic view point, the dosage of cicletanine should only be slightly reduced in patients with a glomerular filtration rate below 30 ml min-', ii) as with most of the diuretic agents, its natriuretic properties were markedly decreased in these patients and iii) an alteration in the renal synthesis of prostacyclin or thromboxane seems unlikely to participate in the pharmacological effects of cicletanine.

show abstract

A new technique for the measurement of urinary 6-keto-prostaglandin F1α: normal values in adults

Cited by 24 publications

References 18 publications

BLOOD PRESSURE EFFECTS OF THROMBOXANE A₂ BLOCKADE IN SPONTANEOUSLY HYPERTENSIVE RATS

BLOOD PRESSURE EFFECTS OF THROMBOXANE A₂ BLOCKADE IN SPONTANEOUSLY HYPERTENSIVE RATS

Atrial natriuretic peptide and urinary prostaglandins in man.

Influence of renal insufficiency on the pharmacokinetics of cicletanine and its effects on the urinary excretion of electrolytes and prostanoids.

Contact Info

Product

Resources

About

A new technique for the measurement of urinary 6-keto-prostaglandin F1α: normal values in adults

Cited by 24 publications

References 18 publications

BLOOD PRESSURE EFFECTS OF THROMBOXANE A2 BLOCKADE IN SPONTANEOUSLY HYPERTENSIVE RATS

BLOOD PRESSURE EFFECTS OF THROMBOXANE A2 BLOCKADE IN SPONTANEOUSLY HYPERTENSIVE RATS

Atrial natriuretic peptide and urinary prostaglandins in man.

Influence of renal insufficiency on the pharmacokinetics of cicletanine and its effects on the urinary excretion of electrolytes and prostanoids.

Contact Info

Product

Resources

About

BLOOD PRESSURE EFFECTS OF THROMBOXANE A₂ BLOCKADE IN SPONTANEOUSLY HYPERTENSIVE RATS

BLOOD PRESSURE EFFECTS OF THROMBOXANE A₂ BLOCKADE IN SPONTANEOUSLY HYPERTENSIVE RATS