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1. The in vitro uptake of ²²Na and ⁴²K was measured simultaneously in rat adenohypophyses during hormone release produced by several secretagogues and during inhibition of hormone release in Ca-free media.

2. Intracellular adenohypophysial [Na⁺] and [K⁺] changed only slightly when the uptake changed. This would indicate that relative permeability changes were the primary effect of the treatments.

3. The uptake of ⁴²K was increased by elevated external [K⁺], but was unaffected by the presence or absence of Ca²⁺. Acid extracts of hypothalamus-stalk—median eminence or cerebellum also increased the ⁴²K uptake.

4. The uptake of ²²Na or ²⁴Na was decreased by elevated [K⁺]. Uptake was increased in Ca-free Krebs—Ringer bicarbonate; but was unaltered when [K⁺] was concurrently increased.

5. Neither purified growth hormone releasing hormone, synthetic lysine-vasopressin, dibutyryl cyclic AMP nor theophylline had an effect on the uptake of either K⁺ or Na⁺.

6. The rapid uptake of ²²Na and its smaller volume of distribution compared to absolute measurements of intracellular [Na⁺] suggest that the plasma membrane of adenohypophysial cells is relatively impermeable to Na⁺.

7. We conclude that changes in the uptake of Na⁺ and K⁺ associated with hormone release are incidental to the release process.

8. Hormone release produced by elevated external [K⁺] is most likely due to a non-specific increase in permeability of the cell membranes, facilitating Ca²⁺ entry into the cytoplasm.

9. The results suggest that the low resting transmembrane potentials of adenohypophysial cells may be due to their conjoint relatively high permeability to both K⁺ and Ca²⁺, rather than K⁺ and Na⁺.