Regulation of the Na, K‐ATPase activity of Madin‐Darby Canine Kidney cells in defined medium by Prostaglandin E1 and 8‐bromocyclic AMP

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Abstract
The role of PGE1 in regulating the activity of the Na+, K+ ‐ATPase in Madin Darby Canine Kidney (MDCK) cells has been examined. PGE1 increased the initial rate of ouabain‐sensitive Rb+ uptake by MDCK cells, a process that continued to occur over a 5‐day period The increase in the initial rate of ouabain‐sensitive Rb+ uptake in MDCK cells treated with PGE1 could be explained by a 1.6‐fold increase in the Vmax for ouabain‐sensitive Rb+ uptake. The increase in the Vmax for ouabain‐sensitive Rb+ uptake observed in MDCK cells under these conditions can be explained either by an increase in the number of active Na+ pumps, or by an increase in the efficiency of the Na+ pumps. Consistent with the former possibility is the observed increase in the number of ouabain binding sites, as well as the increase in Na+, K+‐ATPase activity in cell lysates obtained from MDCK monolayers treated with PGE1. The involvement of cyclic AMP in mediating these effects of PGE1 on the Na+, K+‐ATPase in MDCK cells is supported by: (1) the observation of similar effects in 8‐bromocyclic AMP treated MDCK monolayts, and (2) a dramatic reduction of the stimulatory effects of PGE1 and 8‐bromocyclic AMP on the Vmax for ouabain‐sensitive Rb+ uptake, and on the number of ouabain binding sites in dibutyryl cyclic AMP resistant clone 3 (DBr 3) (which is defective in cyclic AMP dependent protein kinase activity). PGE1 independent MDCK monolayers exhibit both an increase in the Vmax for ouabain‐sensitive Rb+ uptake and an increase in the number of ouabain binding sites in response to 8‐bromocyclic AMP. Apparently, the cyclic AMP phosphodiesterase defect in these PGE1 independent cells did not cause cellular cyclic AMP levels to be elevated to a sufficient extent to maximally increase the Na+, K+‐ATPase activity in these variant cells.

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