6-keto Prostaglandin F_1α ELISA Kit

Prostacyclin (Prostaglandin I₂; PGI₂) is formed from arachidonic acid primarily by the vascular endothelium and renal cortex.^1,2 It is a potent vasodilator and inhibitor of platelet aggregation.² PGI₂ is non-enzymatically hydrated to 6-keto PGF_1α (t_½ = 2-3 minutes), and then quickly converted to the major metabolite, 2,3-dinor-6-keto PGF_1α (t_½ = 30 minutes).^3,4,5 Prostacyclin was once thought to be a circulating hormone that regulated platelet-vasculature interactions, but the rate of secretion into circulation coupled with the short half-life indicate that prostacyclin functions locally.⁶ Although 6-keto PGF_1α is commonly measured in plasma and urine as an estimate of prostacyclin synthesis, it should be noted that there may be more than one source of PGI₂ in these samples. For instance, venipuncture may cause the release of prostacyclin which will artifactually increase the 6-keto PGF_1α concentration in plasma.⁷ Urinary concentrations of 6-keto PGF_1α are confounded by the fact that some plasma prostacyclin (~14%) is excreted into urine as 6-keto PGF_1α and the remainder is of renal origin.^6,7 Therefore, it is important to take these factors into account when analyzing data.

Needed but not supplied: Please download the kit booklet to verify if UltraPure Water (Milli-Q or equivalent) or any other components are needed for this assay.

WARNING This product is not for human or veterinary use.

1. Moncada, S., Gryglewski, R., Bunting, S., et al. An enzyme isolated from arteries transforms prostaglandin endoperoxides to an unstable substance that inhibits platelet aggregation. Nature 263(5579), 663-665 (1976).

2. Navamani, M., Morgan, M., and Williams, R.J. Ethanol modulates N-methyl-D-aspartate-evoked arachidonic acid release from neurones. Eur. J. Pharmacol. 340, 27-34 (1997).

3. Samuelsson, B., Goldyne, M., Granström, E., et al. Prostaglandins and thromboxanes. Annu. Rev. Biochem. 47, 997-1029 (1978).

4. Dusting, G.J., Moncada, S., and Vane, J.R. Prostacyclin (PGX) is the endogenous metabolite responsible for relaxation of coronary arteries induced by arachidonic acid. Prostaglandins 13, 3-15 (1977).

5. Rosenkranz, B., Fischer, C., Reimann, I., et al. Identification of the major metabolite of prostacyclin and 6-ketoprostaglandin F_1α in man. Biochim. Biophys. Acta 619(2), 207-213 (1980).

6. Frolich, J.C. Measurement of eicosanoids. Prostaglandins 27, 349-369 (1984).

7. Catella, F., Nowak, J., and Fitzgerald, G.A. Measurement of renal and non-renal eicosanoid synthesis. Am. J. Med. 81, 23-29 (1986).

Letite, L.N., Gonzafa, N.A., Tirapelli, D.P.C., et al. Pharmacological characterization of the relaxant effect induced by adrenomedullin in rat cavernosal smooth muscle. Braz. J. Med. Biol. Res. 47(10), 876-885 (2014).

Sobrino, A., Mata, M., Laguna-Fernandez, A., et al. Estradiol stimulates vasodilatory and metabolic pathways in cultured human endothelial cells. PLoS One 4(12), e8242 (2009).

Herrerias, A., Torres, R., Serra, M., et al. Activity of the cyclooxygenase 2-prostaglandin-E prostanoid receptor pathway in mice exposed to house dust mite aeroallergens, and impact of exogenous prostaglandin E₂. J. Inflamm. (Lond) 6, 30 (2009).