Analysis of Prostaglandin F2a, and Metabolites in Blood during Constant Intravenous Infusion of Prostaglandin F2a, in the Human Female

Béguin, François; Bygdeman, M.; Gréen, K.; Samuelsson, Bengt; Toppozada, M.; Wiqvist, N.

doi:10.1111/j.1748-1716.1972.tb05349.x

Cited by 51 publications

(11 citation statements)

References 10 publications

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“…Reagents [1-14 C]PGF 2 « (56 mCi/mmol) and [1][2][3][4][5][6][7][8][9][10][11][12][13][14] C]PGE 2 (56 mCi/ mmol) were purchased from the Radiochemical Centre (Amer- 1 Due to the complex nomenclature of successive PG metabolites, the following abbreviations have been used in order to simplify the text: 15-keto-PGE 2 , EMI; 13,14-dihydro-15-keto-PGE 2 , EM2; 13,14-dihydro-15-keto-PGA 2 andl3,14-dihydro-15-keto-llj8,16^-cyclo-PGE 2 , EM3; 15-keto-PGF 2Q , FMl; 13,14-dihydro-15-keto-PGF 2n , FM2. 13,14-Dihydro-15-keto-PGE 2 is unstable and is converted nonenzymically to the bicyclic derivative 13,14-dihydro-15-keto-ll|8,16£-cyclo-PGE 2 via the intermediate 13,14-dihydro-15-keto-PGA 2 .…”

Section: Methodsmentioning

confidence: 99%

“…Although produced by most tissues throughout the body, concentrations of the primary PGs in the peripheral circulation are extremely low (usually <10 pg/ ml). In contrast, the stable metabolite of PGF 2 «, 13,14-dihydro-15-keto-PGF 2 «, circulates at levels approximately 20-fold higher than this (3). In addition, injected PGs are rapidly metabolized during a single passage through the lungs (4).…”

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confidence: 88%

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Metabolism of Prostaglandins by the Nonpregnant Human Uterus*

Abel

Kelly

1983

The Journal of Clinical Endocrinology & Metabolism

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We investigated the ability of the nonpregnant human uterus to metabolize prostaglandins E2 and F2 alpha (PGE2 and PGF2 alpha) using radiolabeled substrates together with gas chromatography-mass spectrometry for the measurement of specific metabolites. Both the 15-hydroxyprostaglandin dehydrogenase and the delta 13-reductase enzymes are present in endometrium and myometrium. As shown for other tissues, the dehydrogenase is NAD+ dependent, while the delta 13-reductase requires NADPH as cofactor. PGE2 was the preferred substrate in both tissues; however, the metabolizing capacity of follicular phase myometrium was comparable with that of midluteal phase endometrium. The Km values of the dehydrogenase for PGE2 and PGF2 alpha were similar in both endometrium (1.89 X 10(-6) and 18.52 X 10(-6) mol/liter, respectively) and myometrium (2.76 X 10(-6) and 11.64 X 10(-6) mol/liter, respectively), suggesting that the same enzyme is present in both tissues although the regulation of this enzyme may differ in endometrium and myometrium.

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Section: Methodsmentioning

confidence: 99%

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confidence: 88%

Metabolism of Prostaglandins by the Nonpregnant Human Uterus*

Abel

Kelly

1983

The Journal of Clinical Endocrinology & Metabolism

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“…This metabolite (PGE2-M) is more stable than the primary prostaglandin and thus may more accurately reflect the cellular biosynthesis of PGE2 (11). Accordingly, the plasma concentration of PGE2-M was measured in peripheral blood by radioimmunoassay.…”

Section: Methodsmentioning

confidence: 99%

Captopril-induced Changes in Prostaglandin Production

Swartz¹,

Williams²,

Hollenberg³

et al. 1980

J. Clin. Invest.

328

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A B S T R A C T Captopril is a potent hypotensive agent whose efficacy has hitherto been attributed to its ability to alter either angiotensin II formation or kinin degradation. Our purpose was to examine captopril's acute effect on prostaglandin production, because changes in neither the renin-angiotensin nor the kallikrein-kinin systems appear adequate to account for the fall in arterial pressure. The plasma levels of' angiotensin II, kinins, and prostaglandins were determined in response to increasing doses (5, 12.5, and 25 mg) of captopril and these responses were compared with the change in arterial pressure observed in nine supine normal male subjects studied on both a high (200 meq) and low (10 meq) sodium intake.Captopril significantly (P < 0.01) increased the levels of the 13,14-dihydro-15-keto metabolite of prostaglandin E2 (PGE2-M), a potent vasodilator, with similar responses being observed on both a high aind a low sodium intake. No significant changes in the plasma levels of 6-keto-prostaglandin F,a, or thromboxane B2, the stable products of prostacyclin and thromboxane A2, respectively, occurred.The depressor response to captopril correlated with the change in PGE2-M (r = 0.52, t = 5.44, P < 0.0001). On the other hand, although significant (P < 0.02) decrements in angiotensin II and increments in plasma kinins accompanied the hypotensive response in sodium-restricted subjects, in sodium-loaded subjects where the renin-angiotensin system was suppressed, nio change in angiotensin II, and only a modest change in kinins was noted, even though significant (P < 0.01) decrements in diastolic blood pressure occurred (-10+2 mm Hg).Thus, changes in depressor prostaglandin production can better account for the hypotensive response to

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“…PG E ,-M is more stable than P G E 2, and thus may more accurately reflect the cellular biosynthesis of P G E 2 [28]. Blood was withdrawn into a chilled plastic syringe and transferred to a heparinized tube al 0 'C .…”

Section: Methodsmentioning

confidence: 99%

Plasma Kinin Levels in Acute Renovascular Hypertension in Dogs

Moore¹,

Gagnon²,

Verma³

et al. 1984

Kidney Blood Press Res

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The role of kinins in the hypertensive response to acute renal artery constriction (RAC) was examined in the dog. RAC resulted in an increase in systemic arterial pressure (SAP) from 144 ± 6 to 155 ± 4 mm HG (p < 0.05). Simultaneously, arterial plasma bradykinin decreased from 2.3 ± 0.2 to 1.4 ± 0.1 ng/ml (p < 0.01), while renal venous bradykinin remained unchanged (2.3 + 0.2 to 2.0 + 0.4 ng/ml, p > 0.05). At the same time urinary kallikrein decreased from 55 ± 6 to 33 + 4 milliesterase units (mEU)/min (p < 0.05), while urinary kinin decreased from 3.2 + 0.4 to 1.9 + 0.3 ng/min (p < 0.05). There was a significant correlation between the decrease in arterial bradykinin and the rise in SAP induced by RAC (p < 0.01). Administration of the dipeptidyl hydrolase inhibitor SQ20881 during RAC reduced angiotensin-converting enzyme levels from 578 + 86 to 10 + 0.0 mU/ml (p < 0.005). There was an associated increase in arterial bradykinin (1.4 + 0.1 to 5.8 ± 0.8 ng/ml, p < 0.001), renal venous bradykinin (2.0 + 0.4 to 5.7 ± 0.5 ng/ml, p < 0.005), and urinary kinin (1.9 ± 0.3 to 5.0 ± 0.7 ng/min, p < 0.01) in conjunction with return of SAP to control levels. Urinary kallikrein, however, remained depressed following SQ20881 (33 ± 4 to 30 ± 5 mEU/min, p > 0.05). These results suggest that (1) decreases in circulating BK may potentiate the vasoconstrictor effect of angiotensin II and contribute to the hypertension induced by RAC, and (2) urinary kallikrein is an unreliable marker of changes in plasma bradykinin in this model of hypertension.

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Analysis of Prostaglandin F_2a, and Metabolites in Blood during Constant Intravenous Infusion of Prostaglandin F_2a, in the Human Female

Cited by 51 publications

References 10 publications

Metabolism of Prostaglandins by the Nonpregnant Human Uterus*

Metabolism of Prostaglandins by the Nonpregnant Human Uterus*

Captopril-induced Changes in Prostaglandin Production

Plasma Kinin Levels in Acute Renovascular Hypertension in Dogs

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