The renal medulla is known to be susceptible to hypoxia. It is known that nitric oxide (NO) blockade causes renal vasoconstriction and, subsequently, renal hypoxia especially in the medulla. To examine the interaction between NO and other vasoactive autacoids, we observed the changes of renal interstitial concentrations of prostaglandin E
2 (PGE
2), adenosine (Ade) and angiotensin II (AgII) following NO inhibition with N
ω-nitro-L-arginine methyl ester (L-NAME: 2 mg/kg) in 7 mongrel dogs. The microdialysis technique (hollow fibre membrane of regenerated cellulose, 10 mm long, 222 μmΦ) was utilized for this purpose. Three probes were inserted into each of the cortical and medullary layers separately. Following enough stabilisation period, the dialysate was collected for 2 hours each before and after L-NAME administration intravenously. After NO blockade, blood pressure increased (9±2%), while renal arterial and cortical blood flow decreased (28±5%, 30±4%, respectively). There was a significant increase of PGE
2 both in the cortex (91±16%) and in the medulla (56±19%). In contrast, there was no significant change in concentrations of Ade and AgII. In summary, the present study demonstrates that renal NO blockade elicits a paradoxical increase in PGE
2, and suggests that the increase of medullary PGE
2 concentration after NO blockade may compensate for further reduction of blood flow.
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