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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

A comparison of the effects of prostacyclin and 6-keto-prostaglandin E1 on renin release in the isolated rat and rabbit kidney.

A direct comparison of the relative potencies of the prostaglandins PGI2 and 6-keto-PGE1 to induce renin release was made in the isolated rat kidney, which was perfused with a synthetic medium at constant perfusion pressure. Both prostaglandins stimulated renin release in a dose-dependent manner (0.01 to 1 microM) and with equal potency. Also in the isolated rabbit kidney, PGI2 and 6-keto-PGE1 had the same potency to induce renin release at 1 microM final concentration. Following infusion of 6-keto-PGE1 a small increase of vascular resistance in the rat kidney was observed, whereas in the rabbit kidney no constrictor effect was seen. When perfusates of PGI2 or 6-keto-PGE1-infused rat kidneys were tested for antiaggregatory activity in the ADP induced aggregation of human platelets and compared with authentic standards, the results showed 6-keto-PGE1 passes the kidney essentially unchanged, whereas only 25-40% of the infused PGI2 appear in the venous perfusates, as judged from the recovery of antiaggregatory activity. Analysis of venous perfusates from 3H-PGI2 infused kidneys by high performance liquid chromatography indicates that about 25% of the infused PGI2 remains intact, a major portion of the perfused radioactivity was identified as 6-keto-PGF1 alpha by combined gas chromatography-mass-spectrometry (19). We conclude that the renin-stimulating effect of PGI2 is not secondary to its metabolism to 6-keto-PGE1, as has been suggested in the literature (8).[1]

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