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In the preceding paper (1) experimental depletion of potassium in normal human subjects did not produce an extracellular metabolic alkalosis of the severity which usually occurs in patients with comparable potassium deficits. Much investigative study has been applied to this association but, because of the many factors involved in such patients, the relative importance of such factors in the etiology of this association in man remains unclear.Most of our knowledge of the metabolic derangements induced in mammals by potassium depletion has come from studies in rats (2-12). The depletion in rats is usually accompanied by metabolic alkalosis of varying severity. A hypothesis accounting for the alkalosis has been formulated by Darrow, Cooke and coworkers (2-4) and has been given additional support by the studies of Orloff, Kennedy and Berliner (9). In brief, the loss of potassium from cells is replaced in part by hydrogen ion from extracellular fluid, the latter shift resulting in an intracellular acidosis and an extracellular alkalosis. This primary cellular distortion of acid-base equilibrium is then maintained by the kidney by an enhancement of tubular reabsorption of bicarbonate over that of chloride and the excretion of a relatively acid urine. In these rat studies the absence or presence and degree of alkalosis appear to be related to many variables including the duration and severity of the depletion, the protein content of the diet, the acidbase composition of the diet and the use of desoxycorticosterone in promoting depletion.

The effects of acetazolamide, sodium perchlorate, ouabain, and of iodide loading on the processes controlling I131 and inulin-C14 distribution in the brain and CSF were studied in nephrectomized rats. It was observed that the first three drugs increased the concentration of both iodide and inulin in the brain and CSF after intracisternal administration of the tracers. It was concluded that acetazolamide reduced the rate of formation and flow of CSF, that perchlorate primarily decreased active iodide transport, and that ouabain slightly reduced CSF formation and flow. Iodide loading increased the CSF/plasma iodide ratio, expressed as percent (CSF iodide space), from 1.97 to 42.17, and the comparable values for brain were 2.02 and 11.76, respectively. The results suggest that the primary factors in the control of iodide distribution in the CNS are the following: 1) an active iodide transport system between CSF and blood, 2) limited permeability to iodide of the structures between blood and CSF and between blood and brain, and 3) relatively free diffusion of iodide between brain and CSF.

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