Renal action of progesterone: effect on calcium reabsorption
Recently, the kidney has been reported to be the site of receptors for progesterone. Although the exact segment of the nephron has not been precisely determined, the cortical collecting tubule was suspected, since the hormone displaces bound 3H aldosterone. The aim of the present study was to invest...
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Published in | Molecular and cellular endocrinology Vol. 194; no. 1; pp. 183 - 190 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
Ireland
Elsevier Ireland Ltd
30.08.2002
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Subjects | |
Online Access | Get full text |
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Summary: | Recently, the kidney has been reported to be the site of receptors for progesterone. Although the exact segment of the nephron has not been precisely determined, the cortical collecting tubule was suspected, since the hormone displaces bound
3H aldosterone. The aim of the present study was to investigate the effect of progesterone on calcium (Ca
2+) transport by the renal luminal membranes and to determine the site and mechanisms of action. Incubation of proximal tubules from rabbit kidney with progesterone did not influence Ca
2+ or Na
+ transport by the luminal membranes. In the distal tubules (DT), a 5 min treatment with 10
−11 M of the hormone enhanced 0.5 mM
45Ca uptake from 0.60±0.02 to 0.84±0.08 pmol/μg per 10 s (
P<0.05) in the absence of Na
+ and from 0.26±0.02 to 0.41±0.02 pmol/μg per 10 s (
P<0.01) in the presence of 100 mM Na
+. The dose–response curve showed a biphasic action with a peak at 10
−11 M. Ca
2+ uptake by DT membranes presents dual kinetics. The hormone enhanced the Vmax value of the high affinity component from 0.41±0.05 to 0.57±0.06 pmol/μg per 10 s (
P<0.05). In contrast, incubation of DT with 10
−8 M progesterone decreased 1 mM Na
+ uptake from 0.68±0.03 to 0.53±0.07 pmol/μg per 10 s (
P<0.05). Finally, 10
−11 M progesterone also enhanced Ca
2+ uptake by the DT membranes through a direct nongenomic mechanism. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 |
ISSN: | 0303-7207 1872-8057 |
DOI: | 10.1016/S0303-7207(02)00113-2 |