Ammonia Excretion in Adrenal Insufficiency

Abstract

The adrenal-insufficient dog without salt support shows great impairment of ammonia production in spontaneously occurring acidosis and in the acutely increased acidosis resulting from NH4Cl or sulfate admn. With a severe enough insufficiency without salt support an almost complete renal shutdown may occur when acidosis is acutely increased, but a degree of insufficiency can be established compatible with satisfactory water and total solids excretion while incompatible with normal ammonia formation. Adrenalectomized dogs in apparently comparable states of insufficiency show great individual variations in susceptibility to such renal shutdown. The adrenalectomized dog maintained on 1 mg. DCA daily shows normal ammonia responses, but 0.1 mg. DCA daily is inadequate. A daily dosage of 1 mg./kg. cortisone is somewhat less effective in maintaining ammonia response than is 1 mg. DCA/dog. The presence of adrenal hormones per se is not essential to normal ammonia response, since normal responses were obtained in the salt-supported dog completely lacking in adrenal hormones. Salt depletion per se is not necessarily responsible for the impairment of ammonia response, since normal responses were obtained in the salt-depleted nonadrenalectomized dog. A combination of salt depletion and of lack of adrenal hormones exerts a cumulative effect in depressing the ammonia response. Failure of the salt-depleted adrenal insufficient dog to show normal ammonia excretion in ammonium chloride acidosis is not dependent on a failure, through chloride depletion, to excrete anions, since ammonia excretion is still impaired in ammonium sulfate acidosis, although there is abundant sulfate excretion.