Renal effects of adenosine 3′,5′-cyclic monophosphate and dibutyryl adenosine 3′,5′-cyclic monophosphate: Evidence for a role for adenosine 3′,5′-cyclic monophosphate in the regulation of proximal tubular sodium reabsorption

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Abstract

Stable water diuresis was produced in anesthetized, hydrocortisone-treated hypophysectomized dogs by infusion of 2.5% dextrose. Infusion of adenosine 3′,5′-cyclic monophosphate (cyclic AMP) in the left renal artery decreased ipsilaterally glomerular filtration rate (GFR), cortical and non-cortical renal plasma flow, and tended to increase urine flow (V) and free-water clearance (CH2O) despite a decrease in mean arterial pressure. Infusion of dibutyryl adenosine 3′,5′-cyclic monophosphate (dibutyryl cyclic AMP) in the left renal artery increased V and CH2O significantly (P<0.01) bilaterally with essentially no change in GFR, in total renal plasma flow or its cortical and non-cortical components. For each kidney the magnitude of the change in V was similar to the magnitude of the change in CH2O and the change in sodium excretion was trivial. Cyclic AMP probably produced its effects on renal hemodynamics and mean arterial pressure wholly or in part through the action of metabolites such as 5′-AMP and adenosine on the renal and systemic vasculature. The absence of an effect of dibutyryl cyclic AMP on renal hemodynamics and its bilateral effect may be explained by the resistance of this nucleotide derivative to metabolism.

Authors

John R. Gill Jr., Alfred G. T. Casper