Little is known about the distribution of prostaglandin E? (PGE?) and prostacyclin (PGLJ production in the canine kidney. To determine the basal and stimulated profiles of PGE^ and PGI 2 production along the corticomedullary axis of the dog kidney, a slice (0.5 mm thick, 10-50 mg) was obtained from six equally spaced zones along the axis (zone 1, medullary crest; zones 2 and 3, inner medulla; zone 4, outer medulla; and zones 5 and 6, cortex) and was divided into equal halves. One half of the slice was incubated with Krebs-Ringer buffer containing arachidonic acid (6.6xlO~< M), bradykinin (9.4x10"' M), or indomethacin (10~5 M), whereas the remaining half of each slice was similarly incubated in Krebs-Ringer buffer alone. The production of PGEj and 6-keto-PGF la (the stable metabolite of PGI 2 ) was determined by radioimmunoassay. Under basal conditions, both PGF^ and 6-keto-PGF la were highest in the innermost zones of the inner medulla (PGEj, 3,328±549 pg/mg; 6-keto-PGF,,,, 1,611±129 pg/mg) and decreased exponentially to low levels in the cortex (PGEj, undetectable; 6-keto-PGF la , 13±2 pg/mg); this production was inhibited by indomethacin. Arachidonic acid significantly increased the production of PGEj in all zones of the kidney and the production of 6-keto-PGF, a only in zones 3 -6 . Bradykinin significantly stimulated production of PGE? in zones 1, 3, and 4 and 6-keto-PGF lCT in zones 4-6, suggesting that in the inner medulla, unlike the cortex, 6-keto-PGF, a production was saturated under basal conditions and could not be stimulated further. PGEj production, on the other hand, was increased throughout all zones of the kidney with excess substrate (arachidonic acid) but was most sensitive to stimulation by bradykinin in the inner medulla. (Hypertension 1990;15(suppl I):I-107-I-lll)
Adenosine is a renal vasoconstrictor that plays an important role in mediating renal adaptive responses to decreases in renal perfusion pressure. It is known that adenosine acts on the metabolism of arachidonic acid, but the direct repercussions of adenosine in the production of renal prostaglandins and leukotrienes have not been studied. This study was undertaken to evaluate the effect of the intrarenal infusion of adenosine upon the urinary elimination of arachidonic acid derivatives. Samples of urine were collected with lysine acetylsalicylate and determination of prostaglandins (PGs) and leukotrienes (LTs) was performed by radioimmunoassay of samples previously separated by HPLC. The infusion of adenosine decreases the urinary excretion of 6-keto-PGF1α and TxB2 significantly. There was no significant change in urinary excretion of PGE2 while LTB4 and LTC4 showed a tendency to increase. These results suggest that a fall in the synthesis of PGI2 along with an increase in LTC4, which is a constrictor of mesangial cells, could be responsible for the renal vasoconstriction phase of adenosine. Therefore, it was concluded that adenosine vasoconstriction is mediated through the inhibition of the cyclo-oxygenase pathway, diminishing the synthesis of PG vasodilators.
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