ADH-PGE2 interactions in cortical collecting tubule. II. inhibition of Ca and P reabsorption

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Abstract
In the absence of ADH [antidiuretic hormone], microperfused cortical collecting tubules of rabbits reabsorb Ca and P. Antidiuretic hormone (ADH) (200 .mu.U/ml Pitressin or synthetic arginine vasopressin) inhibits the reabsorption and may promote the secretion of Ca and P. At 5 min after incubation with ADH, there was a transitory increase in the potential difference and the reabsorption of Na. The fluxes of Ca and P showed no significant change from the control values. At 30-50 min after treatment with ADH, the reabsorption of Ca and P was inhibited and in some tubules Ca and P were secreted. The removal of vasopressin from the bath or the addition of 10-5 M meclofenamate to the bath containing ADH returned ionic fluxes to control levels of reabsorption. Pretreatment of tubules with meclofenamate in vitro prevented ADH from inhibiting the reabsorption of Ca and P. Treatment of tubules with 10-5 M prostaglandin (PG)E2 subsequent to incubation in a medium containing ADH and meclofenamate inhibited the reabsorption or even promoted the secretion of Ca and P, as did the prolonged incubation with ADH alone. Cortical collecting tubules reabsorb Ca and P in the absence of vasopressin and ADH inhibits Ca and P reabsorption. Endogenous synthesis of PGE2 may mediate the inhibitory action of ADH, since meclofenamate (an inhibitor of the synthesis of PG) opposes and exogenous PGE2 mimics ADH.

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