Reference

Measurement of prostaglandin D2 and identification of metabolites in human plasma during intravenous infusion

Measurement of prostaglandin D2 and identification of metabolites in human plasma during intravenous infusion. Barrow, S. E.; Heavey, D. J.; Ennis, M.; Chappell, C. G.; Blair, I. A.; Dollery, C. T. (R. Postgrad. Med. Sch., Hammersmith Hosp., London W12 0HS, UK). Prostaglandins, 28(6), 743-54 (English) 1984. CODEN: PRGLBA. ISSN: 0090-6980. DOCUMENT TYPE: Journal CA Section: 2 (Mammalian Hormones) A stable isotope diln. assay was developed for the detn. of PGD2 [41598-07-6] in plasma. Samples were analyzed by capillary column gas chromatog./neg. ion chem. ionization mass spectrometry (GC/NICIMS). The method employs an internal std. of [2H6]PGD2., prepd. biosynthetically by incubation of rat peritoneal mast cells with deuterated arachidonic acid. No PGD2 was detected in peripheral venous plasma samples obtained from healthy male volunteers (detection limit = 5 pg/mL). Following i.v. infusion of PGD2 at increasing incremental infusion rates ranging 16-256 ng/kg/min, a dose-related increase in the plasma concn. of PGD2 was obsd. Plasma levels at 128 ng/kg/min ranged 724-1444 pg/mL. The major circulating metabolites of PGD2, during infusion, were identified as 13,14-dihydro-15-oxo-PGF2a [27376-76-7] and 15-oxo-PGF2a [35850-13-6].

Comparison of renal prostaglandin and p-aminohippuric acid transport processes

Comparison of renal prostaglandin and p-aminohippuric acid transport processes. Bito, Laszlo Z.; Baroody, Roger A. (Coll. Physicians Surg., Columbia Univ., New York, N. Y., USA). Am. J. Physiol., 234(1), F80-F88 (English) 1978. CODEN: AJPHAP. ISSN: 0002-9513. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacodynamics) Section cross-reference(s): 13 Isolated rabbit kidneys were perfused with Krebs-Henseleit soln. contg. 3H-labeled PGF2a [551-11-1] and inulin-14C or 14C-labeled p-amino hippuric acid PAH [61-78-9]. The org. acids, bromcresol green [76-60-8], probenecid [57-66-9], indomethacin [53-86-1], as well as the PGF2a metabolite, 15-keto-PGF2a [35850-13-6], and the prostaglandin antagonist, diphloretinphosphate [39201-04-2], showed a 50% inhibition (I50) of both the PGF2a (or PG metabolite) and the PAH transports in the range of 2-6 mM. With the exception of bromcresol green, this inhibition was readily reversible. PGF2b [4510-16-1], furosemide [54-31-9] tetraethylammonium chloride [56-34-8] and penicillin G [61-33-6] also had a similar inhibitory effect on both prostaglandin and PAH transports with an I50 in the range of 16-75 mM. Paracetamol [103-90-2], aspirin [50-78-2], iodipamide [606-17-7], PAH, and phenelzine [51-71-8] had an I50 effect on these transports only in the range of 0.2-3.4 mM. Inulin excretion rates were not inhibited. In the presence of 10-3M PAH, PGF2b completely inhibited the residual PAH transport at a concn. of 10-6M, whereas the residual PG transport was not completely inhibited even at a 10 times higher PGF2b concn. Bolus isotope injection and stop-flow expts. showed that the passage of prostaglandinsand/or their metabolites into the urine was delayed compared to the passage of PAH. Only one PGF2a metabolite was found in the venous effluents by paper chromatog. while at least 5 metabolites were present in all 3H-contg. urine samples. A shift toward less polar metabolites was apparent in later as compared to the 1st urine fractions. The effective renal excretion of prostaglandins and/or their metabolites is clearly dependent on a tubular transport system that shows some similarities to the classical PAH transport system, but is exptly. distinguishable from it. It is concluded that the renal PG transport system represents a subclass of the classical org. acid transport system.