TITLE

The cAMP system in vasopressin-sensitive nephron segments of the vitamin D-treated rat

AUTHOR(S)
Berl, Tomas
PUB. DATE
May 1987
SOURCE
Kidney International;May1987, Vol. 31 Issue 5, p1065
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
The present study was undertaken to investigate the cAMP system in isolated vasopressin CAVP)-sensitive segments of the hypercalcemic rat. Hypercalcemia was produced by supplementation of diet with dihydrotachysterol, achieving a mean serum calcium of 12.6 mg%. Maximal urinary concentration was only 1982 ± 119 mOsm/kg H2O in pair, watered hypercalcemic rats when compared to 2478 ± 93 mOsm/kg H2O in controls (N = 7) (P < 0.01). Vasopressin stimulated adenylate cyclase activity at concentrations of vasopressin between 10-9 and 10-7 M was indistinguishable in the outer medullary collecting duct (OMCD) and inner medullary collecting duct (IMCD) of tubules dissected from hypercalcemic rats or normocalcemic rats. Likewise, in situ cAMP accumulation in response to 10-7 M AVP was not significantly different in either OMCD or IMCD of hypercalcemic or normocalcemic rats at either isotonic or hypertonic media conditions. In contrast, while 10-7 M AVP significantly (P < 0.05) increased cAMP accumulation in the medullary ascending limb (MAL) of normocalcemic rats it failed to do so in the MAL of hypercalcemic rats. This failure to accumulate cAMP appears to be due to impairment in AVP-stimulated adenylate cyclase rather than to enhanced phosphodiesterase activity. A similar decrement in glucagon stimulated adenylate cyclase occurred with 10-6 M glucagon. The results demonstrate that in chronic hypercalcemia the cAMP system in the OMCT and IMCD of the rat is intact, but the MAL demonstrates abnormal AVP responsiveness due to impaired adenylate cyclase. Such an effect in the MAL may explain the decreased medullary-solute content in hypercalcemia and thereby contribute to the concentrating defect seen in the vitamin D treated rat.
ACCESSION #
17676151

 

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