R. Fransen et Ha. Koomans, ADENOSINE AND RENAL SODIUM HANDLING - DIRECT NATRIURESIS AND RENAL NERVE-MEDIATED ANTINATRIURESIS, Journal of the American Society of Nephrology, 6(5), 1995, pp. 1491-1497
Adenosine infusion is associated with natriuresis as well as antinatri
uresis. The physiologic significance of these opposite effects is unkn
own but may have to do with different conditions of ischemia, in which
adenosine accumulates. These effects were characterized in the rat. F
irst, intrarenal and systemic infusions within one animal were perform
ed, Infusing 10 mu g/min into the left renal artery increased sodium b
y similar to 50%; however, the subsequent infusion of 50 mu g/min into
the thoracic aorta decreased sodium excretion by similar to 60%, in a
ssociation with a small reduction of blood pressure. Second, to explor
e the effect of intrarenal adenosine on tubular sodium handling, free-
flow micropuncture experiments were performed. The intrarenal infusion
of 10 mu g/min again caused sodium excretion, but no change in GFR, v
olume, and sodium deliveries up to the early distal tubule was found.
Apparently, the direct effect of adenosine in the kidney is sodium exc
retion, by a tubular action beyond the early distal tubule. Third, to
further characterize the indirect effect, which apparently is sodium r
etention, adenosine was infused systemically at low rates, in order to
avoid a decrease in blood pressure. A 25 mu g/min infusion again caus
ed sodium retention, in the absence of a fall in blood pressure. After
acute left renal denervation, the antinatriuretic effect disappeared
in the denervated kidney but remained in the right kidney. These data
suggest that increased intrarenal adenosine suppresses sodium reabsorp
tion at some distal nephron site, appropriately decreasing the workloa
d of the kidney. On the other hand, systemic adenosine stimulates sodi
um reabsorption, an effect that is appropriate to improve systemic cir
culation and depends on the renal nerves.