Studies were performed to determine whether cAMP impairs prostaglandin (PG) E2 production in a homogeneous population of cultured rat inner medullary collecting duct cells. Three structurally different cAMP analogues were shown to decrease PGE2 synthesis by 48.4% in the basal state and by 49.3% in response to the divalent cation ionophore A23187 (5 microM). Thromboxane B2 production was similarly suppressed. An increase in endogenous cAMP by forskolin also decreased PGE2 synthesis. To determine the locus of the cAMP effect we examined the response to exogenously added arachidonic acid. At a concentration of arachidonic acid (5 micrograms/ml) sufficient to render the phospholipase-dependent fraction negligible (as evidenced by the lack of a mepacrine effect), cAMP had no effect on PGE2 production, suggesting phospholipase as the site of cAMP action. Further evidence for a phospholipase-mediated mechanism derives from studies employing [5,6,8,9,11,12,14,15-3H(N)]arachidonic acid in which cAMP analogues had no effect on the rate of cellular arachidonic acid incorporation, but did impair the release of tritiated arachidonic acid in response to ionophore. These results suggest the existence of a negative feedback system that, by impairing phospholipase activity and PGE2 synthesis, could enhance the action of cAMP in the antidiuretic state.
declared that, 'The evidence is here,' in reference to a Wyeth product. These bands convey the impression of a connection between scientific evidence for the products, the pharmaceutical company, and the independent academic journal.The November editions of the Journal of the American Society of Nephrology, American Journal of Kidney Diseases, and Kidney International contained 30, 19, and 13 advertisements, respectively. Of these three journals, the November issue of Kidney International actually had the lowest number of large page advertisements. However, unlike these other journals, advertisements in Kidney International were not limited to the pages preceding and following the contents of the journal but were interspersed. These observations raise the question of whether journals face a trade-off between running a larger number of appropriate advertisements or a lesser number of (presumably more lucrative) inappropriate advertisements in order to cover costs.To avoid risking the loss of respect of its readers, we urge Kidney International to eliminate practices that blur the boundary between academic pursuits and advertising. If we are incapable of self-regulation, it will only be a matter of time before the government steps in to control advertising practices in medical journals.
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