Renal Prostaglandin Efflux Induced by Vasopressin, Ddavp and Arachidonic Acid: Contrasting Profile and Sites of Release

Abstract

Prostaglandin (PG) efflux into ureteral (UE) and venous effluents (VE) of rabbit isolated perfused kidneys was determined by superfusion bioassay and radioimmunoassay (RIA), in response to injections of arginine-vasopressin (AVP), the non-pressor vasopressin analogue 1-deamino-8-D-arginine vasopressin (dDAVP) and arachidonic acid (AA). dDAVP (10-1000 ng) failed to stimulate renal PG release, whereas AVP (10-100 ng) and AA (10-50 micrograms) caused a dose-dependent release of PG. AVP evoked PG release into both effluents with release into the VE greater than UE at high doses. In contrast, PG release by AA was almost exclusively into the VE. Indomethacin (2.8 X 10(-6) mol/l) abolished AVP- and AA-induced PG efflux in both effluents, and vasodepressor responses to AA. PGE2 was the predominant PG released in response to AVP in both effluents whereas AA released primarily 6-keto-PGF1 alpha. The contrasting sites and profile of released PG suggest that exogenous AA and AVP stimulate the release of PG from different regions/cell types within the kidney.

Prostaglandin E2 systemic production in patients with asthma with and without aspirin hypersensitivity

“…Local biosynthesis of PGE 2 , dependent on both constitutive COX-1 and inducible COX-2 in the kidneys, varies with age and salt intake. It is also affected by several drugs including angiotensin converting enzyme inhibitors 20. PGE 2 produced in the kidneys is excreted as the parent compound and does not affect the pool of metabolites produced by systemic inactivation of PGE 2 21.…”

Effects of endogenous and synthetic prostanoids, the thromboxane A2 receptor agonist U‐46619 and arachidonic acid on [3H]‐noradrenaline release and vascular tone in rat isolated kidney

“…The marked postjunctional effect of arachidonic acid would then be possibly due to a production of PGI2 and PGF24. Indeed, in the rabbit kidney (Miller et al, 1986) the main prostaglandins formed from exogenous arachidonic acid infused into the renal artery were PGF2. and PGI2, the latter measured as the stable metabolite PGFj..…”

“…They have been shown to be released from the kidney by renal nerve stimulation (RNS) (Needleman et al, 1974) and through activation of al-adrenoceptors by exogenous al-adrenoceptor agonists (Cooper & Malik, 1985). Moreover, prostaglandins can be formed locally in the kidney from exogenous arachidonic acid (Miller et al, 1986). Generally it has been shown that prostaglandins, mainly prostaglandin E2 (PGE2), inhibit noradrenaline release by activating prejunctional inhibitory prostaglandin receptors (Starke, 1977;Hedqvist, 1977).…”