These studies are designed to test the hypothesis that parathyroid hormone (PTH) acts as a naturally occurring calcium ionophore in the toad bladder. The hormone inhibits vasopressin-stimulated water flow in toad bladder in concert with an increase in Ca45 uptake. The effect is seen at 1 nanogm/ml, a level close to the physiologic range reported for the hormone in vivo. High concentrations of PTH stimulate basal water flow. The effect of PTH on vasopressin-stimulated water flow is lost following prostaglandin inhibition and if the bladders are bathed in low calcium medium. Synthetic 1-34 PTH, in high concentrations, also inhibits vasopressin-stimulated water flow. The hormone also inhibits sodium transport in toad bladder. One part of this grant is designed to examine further the cellular mechanisms whereby PTH inhibits water and sodium transport in the toad bladder. This proposal also intends to elucidate the mechanism by which calcium is transported across the isolated turtle bladder membrane. Under control conditions the net calcium flux is a secretory on (i.e., serosa to mucosa). Following ouabain the net calcium flux totally reverses (i.e., from mucosa to serosa). The mechanisms for these observations are unknown. As both the toad and turtle urinary bladders are analogues of the mammalian collecting duct, these studies will give fundamental information as to the mechanism of parathyroid hormone action, the role of calcium in sodium and water transport, and the mechanisms of transepithelial calcium transport.
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