Parathyroid hormone inhibits water flow in the isolated toad bladder

These experiments studied the effect of parathyroid hormone (PTH) (1-84) on water and Ca transport in isolated toad bladder sacs and toad bladder epithelial cells. Serosal addition of PTH significantly inhibited maximal water flow induced by vasopressin or exogenous cyclic AMP. This effect was seen over a wide range of concentrations, with the threshold for the effect occurring at 1 ng/ml. Pretreatment of the toad bladder sacs with prostaglandin inhibitors (indomethacin or ibuprofen, 1 X 10(-6) M) or preincubation in low-Ca medium (0.089 mM) abolished the effect of PTH on vasopressin-stimulated water flow. Pretreatment of the toad bladders with lanthanum (5 X 10(-5) M) also abolished the effect of PTH on vasopressin-stimulated water flow. Synthetic PTH (1-34) inhibited vasopressin-stimulated water flow only at a high concentration (1 microgram/ml). PTH increased 45Ca uptake by toad bladder epithelial cells but had no effect on 45Ca efflux. These results demonstrate that PTH inhibits water transport beyond the generation of cyclic AMP. That the effect of PTH was abolished in a low-Ca medium or by pretreatment with lanthanum suggests that cell Ca uptake is required for the effect of PTH on water transport. That prostaglandin inhibitors also block the effect of PTH on vasopressin-stimulated water flow suggests that prostaglandin synthesis is required for the effect. These data suggest that the effect of PTH on water flow is mediated by an increased cellular uptake of Ca that stimulates prostaglandin release. Prostaglandin release, in turn, appears to mediate the inhibitory effect of PTH on vasopressin-stimulated water transport.(ABSTRACT TRUNCATED AT 250 WORDS)