help button home button Endocrine Society Endocrinology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kinoshita, Y.
Right arrow Articles by Fujita, T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kinoshita, Y.
Right arrow Articles by Fujita, T.

Endocrinology, Vol 119, 1954-1963, Copyright © 1986 by Endocrine Society


ARTICLES

Establishment of a parathyroid hormone-responsive phosphate transport system in vitro using cultured renal cells

Y Kinoshita, M Fukase, A Miyauchi, M Takenaka, N Nakada and T Fujita

A new system was established using primary cultured mouse kidney epithelial cells to study the effect of PTH on renal tubular phosphate transport. The cells used in our study had alkaline phosphatase activity. They showed increased cAMP content in response to PTH, calcitonin, and vasopressin. Thus, these cells were thought to be a mixture of cells originating from the proximal and distal renal tubules. To explore the mechanism of phosphate handling in these cells, the accumulation of radioactive phosphate from the medium into the cells and the spaces between the cell layer and culture plate (submonolayer spaces) was measured. The accumulation of phosphate by the cells was a sodium-dependent, energy-dependent process, which was demonstrated by inhibition both in the absence of sodium and in the presence of ouabain or 2,4-dinitrophenol. Furthermore, phosphate accumulation was decreased significantly by PTH presumably acting through cAMP. PTH inhibited phosphate accumulation not by affecting the efflux process, but by affecting the uptake process through the apical membrane of the cultured cells without altering the compartmental mental distribution of the accumulated phosphate. These characteristics of phosphate accumulation resemble those of renal tubular phosphate transport.


This article has been cited by other articles:


Home page
Am. J. Physiol. Renal Physiol.Home page
I. Fernandes, R. Beliveau, G. Friedlander, and C. Silve
NaPO4 cotransport type III (PiT1) expression in human embryonic kidney cells and regulation by PTH
Am J Physiol Renal Physiol, October 1, 1999; 277(4): F543 - F551.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 1986 by The Endocrine Society