Effect of adenosine on the distribution of renal blood flow in dogs.

Abstract

The intrarenal infusion of adenosine causes a relatively greater fall in superficial nephron glomerular filtration rate (GFR) than whole kidney GFR. This nonuniform decrease in GFR occurred despite a concomitant increase in total renal blood flow (RBF). The effect of intrarenally administered adenosine on the distribution of RBF was studied. RBF distribution was measured with radiolabeled microspheres (15 .mu.m) in anesthetized dogs (no. = 8) before and during the intrarenal artery infusion of adenosine (0.3 .mu.mol/min). In dogs with elevated plasma renin activities (PRA) adenosine infusion produced no significant change in outer cortical blood flow (4.36 .+-. 0.50 vs. 4.41 .+-. 0.63 ml/min per g), but absolute inner cortical blood flow increased by 94% (1.54 .+-. 0.34 v. 2.99 .+-. 0.52 ml/min per g). In dogs with low PRA, outer cortical blood flow was only minimally affected by adenosine infusion (6.39 .+-. 0.44 vs. 5.88 .+-. 0.33 ml/min per g), but inner cortical blood flow was increased from 4.91 .+-. 0.43 to 6.06 .+-. 0.38 ml/min per g. Adenosine caused a deep cortical vasodilation in dogs with both high and low PRA (94% vs. 23%), but the relative change was greater in the animals with high PRA. Additional experiments were performed in indomethacin- (or meclofenamate-) treated (no. = 14) or phenoxybenzamine-treated (no. = 5) dogs to determine whether the deep cortical vasodilation is mediated by increased prostaglandin [PG] production or by inhibition of norepinephrine release. The increase in deep cortical flow during adenosine administration was not affected by blockade of PG synthesis or .alpha.-adrenergic receptors. The effect of adenosine to preferentially dilate vessels of the inner cortex is independent of a PG related or sympathetic adrenergic mechanism.