Relationship of adrenocortical and anterior pituitary function to fecal excretion of sodium and potassium

¹ Section of Experimental Cardiovascular Disease, National Heart Institute, Bethesda, Maryland, and the Department of Pathological Anatomy, Mayo Clinic, Rochester, Minnesota
² Section on Experimental Cardiovascular Disease, National Heart Institute, Bethesda, Maryland, and the Department of Pathological Anatomy, Mayo Clinic, Rochester, Minnesota

The relationship of aldosterone excretion in urine to Na and K output in feces was studied. In dogs with thoracic inferior vena cava constriction and ascites, a high rate of urinary aldosterone output was associated with a very low fecal Na/K excretion. Following bilateral adrenalectomy and in the absence of hormone therapy, aldosterone was no longer detectable in urine and fecal electrolyte excretion returned to within normal limits. Hypophysectomy of dogs with thoracic caval constriction and ascites was followed by a decrease in urinary aldosterone and a concurrent rise toward or to normal of the fecal Na/K ratio. The data suggest that increased circulating aldosterone influences the intestinal mucosal transport of Na and K. Also, the effects of hypophysectomy on fecal electrolyte and renal Na excretion were observed in otherwise normal dogs. Fecal Na and K excretion increased following hypophysectomy in the majority of these animals; the increase in fecal Na output was progressive and more pronounced than that in fecal K excretion. Renal Na excretion was low during the early posthypophysectomy period but, subsequently, increased sufficiently for Na balance to be achieved in all but one dog.

Note:
With the Surgical Assistance of Alfred Casper