Studies from our laboratory have shown that the natriuresis of extracellular fluid volume expansion (ECVE) in thyroparathyroidectomized (TPTX) dogs is accompanied by increased production of nephrogenous cyclic AMP (cAMP) with most of it added to the renal vein. Also, renal vasodilatation, per se, in hydropenic TPTX dogs resulted in increased nephrogenous cAMP added to the renal vein and natriuresis. In addition, we have shown that stimulation of renal cAMP by cholera toxin is associated with natriuresis. Furthermore, during caval constriction and blunted natriuresis after ECVE there was no increase in nephrogenous cAMP. The proposed research is designed to continue our efforts to define and delineate the relationships between renal cAMP and renal handling of sodium. More specifically, renal production of cAMP will be measured in TPTX dogs in the following conditions: 1) Various degrees of ECVE and natriuresis; 2) Volume expansion with hyperoncotic albumin; 3) During the use of diuretics and osmotic diuresis; 4) During increased arterial pressure and unilateral renal vasodilatation; 5) During renal vasodilatation and increased arterial pressure in caval dogs and blunted natriuresis. These maneuvers are known to reverse sodium retention in this condition. 6) During renal vasodilatation with various agents that cause variable natriuresis. 7) During ECVE and prevention of the exposure of the kidney to its hemodynamic effects (aortic constriction). 8) During ECVE and prostaglandin inhibition. 9) During the infusion of parathyroid hormone, vasopressin or cholera toxin. 10) During total reinfusion of urine; 11) During chronic expansion with DOCA and high salt intake; 12) During chronic bile duct ligation and sodium retention.