Studies will be undertaken to further study the pathogenesis of abnormal water excretion in pathological states. The renal concentrating defect in hypercalcemia will be completed by attention to derangement at the renal level (tissue tonicity, papillary plasma flow, the cyclic AMP system). The effect of agents that alter cellular calcium uptake such as verapamil and nifedipine on the process will be assessed. The abnormal urinary concentration in the recovery from acute renal failure of both ischemic and nephrotoxic nature will also be evaluated in the same terms. Also the role of renal hemodynamics and persistent vasopressin secretion in the abnormal water excretion in heart failure will be studied. A model of cardiomyopathy employing Adriamycin will be used to this end. Studies on the role of calcium uptake on vascular reactivity will be continued. Experiments employing calcium antagonists will be supplemented by the use of calcium ionophores and vasodilators. These experiments will also be extended to the study of various experimental models of hypertension. Finally, both the pressor and antidiuretic antagonists of vasopressin will be employed. The former compounds will aid in defining the role of vasopressin in the increased systematic pressure of a number of experimental models of hypertension, while the latter will be employed to conclusively define the role of the hormone in the abnormal water excretion in cirrhosis and adrenal insufficiency.
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