Effect of Exogenous Adenosine 3´:5´-Cyclic Monophosphate, Parathyroid Hormone and Acetazolamide on Electrolyte Hormone and Acetazolamide on Electrolyte Excretion by the Isolated Perfused Rat Kidney

Abstract

The effects of exogenous adenosine 3´: 5´-cyclic monophosphate (cyclic AMP), parathyroid hormone (PTH) and acetazolamide (Az) on renal calcium and phosphate excretion of the isolated perfused rat kidney were compared. Both PTH and Az evoked an early increase in urinary cyclic AMP excretion followed by a later more prolonged increase in phosphate excretion. All of the increased urinary cyclic AMP was derived from renal cells. Calcium excretion decreased with PTH but was unchanged with Az. Sodium and potassium excretion increased with Az but not PTH. Transitory urinary cyclic AMP excretion rates following bolus additions of exogenous cyclic AMP to perfusate were up to twentyfold greater than those evoked by PTH or Az but unassociated with changes in calcium, phosphate, sodium or potassium excretion. Sustained perfusate levels (above 0.5 µM) and excretion rates of cyclic AMP induced phosphaturia proportional to the perfusate cyclic AMP concentrations achieved up to 2.0 µM. Clearances of exogenous cyclic AMP exceeded inulin clearance at perfusate concentrations greater than 1.0 µM. Aminophylline evoked a small phosphaturia which increased further on addition of cyclic AMP to 5 µM. Glomerular filtration was not affected by any of the agents except Az. Since increased phosphate excretion could be evoked only at perfusate concentrations exceeding either plasma or intracellular concentrations observed in vivo, it is concluded that circulating cyclic AMP at levels in vivo is unlikely to mediate a significant fraction of the renal effects of PTH.