Adenosine induced fall in glomerular capillary pressure. Effect of ureteral obstruction and aortic constriction in the Munich-Wistar rat kidney.

The effect of acute ureteral obstruction (UO) and reduction of renal artery pressure (AC) on the adenosine-induced renal vasoconstriction was studied in the Munich-Wistar rat. Infusion of adenosine, 0.05 mumol/min . kg body weight, into the thoracic aorta, was associated with a fall of directly measured glomerular capillary pressure (Pgc) from 45.2 + 1.8 to 32.5 + 1.7 mm Hg, P less than 0.001. Elevation of ureter pressure to 39 + 2 mm Hg abolished the fall of Pgc following adenosine infusion, 51.3 + 1.7 vs. 50.0 + 1.3 mm Hg, NS. Reduction of renal artery pressure to 70 mm Hg by an aortic clamp above the renal arteries also prevented the fall of Pgc due to adenosine, 36.8 + 0.9 vs. 36.4 + 1.8 mm Hg, NS. Administration of indometacin (10 mg/kg i.v.) restored the ability of adenosine to reduce Pgc in UO from 41.5 + 1.1 to 25.9 + 2.6 mm Hg (P less than 0.001) and in AC from 34.0 + 3.4 to 28.2 + 75.7 mm Hg (P less than 0.02). Since previous studied have demonstrated that in UO and AC renal prostaglandin synthesis is enhanced the effects of indometacin suggest that prostaglandins could be antagonistic to the action of adenosine on the kidney. The data show that the renal vasculature becomes insensitive to the vasoconstrictive action of adenosine during elevated ureter pressure and reduced renal artery pressure.