Parathyroid hormone has been shown to stimulate cyclic AMP production by the kidney in man and lower animals. Cyclic AMP and parathyroid hormone have also been shown to inhibit reabsorption of sodium and phosphate at the level of the proximal convoluted tubule. Although these effects are well documented the underlying mechanism of action is unknown. The objective of this study is to elucidate the mechanism of action of cyclic AMP on renal transport of sodium and phosphate. Previous work in this laboratory suggests that the mechanism of action of cyclic AMP may be to induce changes in the permeability characteristics of the proximal tubular epithelium. Since net transport represents active transport from tubular lumen to plasma minus any back diffusion from plasma to tubular lumen, inhibition of transport may represent either decreased active transport or increased back diffusion. From previous data which shows a change in tubular permeability it can be hypothesized that transport of sodium and phosphate is inhibited by increased passive back diffusion. To prove this hypothesis it will be necessary to measure simultaneously the unidirectional and net fluxes of sodium and phosphate during control periods and during stimulation with either parathyroid hormone or cyclic AMP. Utilizing micropuncture techniques, the mechanism of action of cyclic AMP and parathyroid hormone will be studied in superficial nephrons of the rat kidney. By microperfusing proximal convolutions with fluids of known concentration and then sampling the perfused fluid at downstream sites, net and unidirectional fluxes for sodium and phosphate transport can be determined. Parathyroid hormone or cyclic AMP should cause a decrease in the net flux with no change in the lumen to plasma unidirectional flux. This experimental design will permit identification of the mechanism by which transport is inhibited and separation of mechanisms if there is a difference.