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  • Title: Jejunal phosphate transport is not regulated by the PTH-adenylate cyclase system. Further studies on the contrasting features between intestinal and renal phosphate transport mechanisms.
    Author: Lee DB, Walling MW, Palant CE, Tallos E.
    Journal: Miner Electrolyte Metab; 1986; 12(5-6):293-7. PubMed ID: 3027518.
    Abstract:
    Direct application of parathyroid hormone (PTH) to renal proximal tubule in vitro stimulates the adenylate cyclase system which in turn causes reduction in phosphate (P) reabsorption. Similar application of parathyroid extract to rat jejunum fails to induce changes in P transport. In the present study we examined the basis for this PTH-unresponsiveness in rat jejunum. The effect of PTH, and another peptide hormone, salmon calcitonin (SCT) and sodium fluoride (NaF) on jejunal adenylate cyclase activity was first examined in both vitamin D-deficient (-D) rats and similar rats after 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] repletion. Jejunal cyclic 3',5'-AMP (cAMP, pmol/mg protein/min) increased from 11.0 +/- 1.1 in -D rats to 23.0 +/- 2.2 in 1,25(OH)2D3-repleted rats (p less than 0.001). Neither PTH nor SCT had any effect on adenylate cyclase activity in jejunum from either -D or 1,25(OH)2D3-repleted rats. NaF caused the anticipated stimulation in cAMP generation, a response independent of the vitamin D nutritional status of the animal [-D: 76.8 +/- 1,25(OH)2D3: 86.9 +/- 8.5]. We then examined the question if exogenous cAMP, which reduces renal P reabsorption, also causes decrease in intestinal P absorption. The effect of dibutyryl cAMP (DbcAMP) on transepithelial, net P absorption was examined in short-circuited jejunal epithelia from rats maximally stimulated by 1,25(OH)2D3. DbcAMP caused the anticipated increase in short-circuit current (+212%) without affecting the net, active P absorption. We conclude that, unlike the renal proximal tubule, the adenylate cyclase system in jejunum is insensitive to PTH, and the P absorptive mechanism is resistant to cAMP.
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