AJP - Endo Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Endocrinol Metab 255: E886-E893, 1988;
0193-1849/88 $5.00
This Article
Right arrow Full Text (PDF)
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
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bringhurst, F. R.
Right arrow Articles by Potts, J. T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bringhurst, F. R.
Right arrow Articles by Potts, J. T., Jr

AJP - Endocrinology and Metabolism, Vol 255, Issue 6 E886-E893, Copyright © 1988 by American Physiological Society

ARTICLES

Peripheral metabolism of PTH: fate of biologically active amino terminus in vivo

F. R. Bringhurst, A. M. Stern, M. Yotts, N. Mizrahi, G. V. Segre and J. T. Potts Jr
Endocrine Unit, Massachusetts General Hospital, Boston 02114.

Clearance of intact parathyroid hormone (PTH) from blood is associated with rapid uptake by liver and kidney, limited proteolysis by tissue endopeptidases and, within minutes, appearance of circulating carboxyl-(COOH)-terminal PTH fragments. The fate of the corresponding amino(NH2)-terminal portion of the hormone during this peripheral metabolism is still unknown, however. To determine this, we have employed [35S]bovine PTH (bPTH) labeled to high specific activity at NH2-terminal methionines, which permits direct monitoring of the fate of the PTH NH2-terminus during metabolism in vivo. The [35S]PTH was administered by bolus or continuous intravenous infusion to anesthetized normal rats, to rats subjected to acute ablation of the liver, the kidneys, or both, and to rats receiving co-infusions of excess synthetic bPTH(1-34) NH2-terminal fragments. Analysis by high-resolution chromatographic techniques sensitive to 10(-13) M [35S]PTH peptides in plasma yields no evidence that peripheral metabolism of PTH generates circulating NH2-terminal fragments, even when special measures are taken to block clearance of such putative fragments from blood. We find that the NH2-terminus of PTH is rapidly degraded in situ by the liver but that both liver and especially kidney nevertheless contain low levels of NH2-terminal PTH fragments that, although not released into the blood, are large enough to be potentially active. Thus, the peripheral metabolism of PTH in normal animals does not normally lead to the formation of circulating amino terminal fragments of the hormone that might act independently of intact PTH on peripheral target tissues.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Cell Physiol.Home page
A. A. Selim, M. Mahon, H. Juppner, F. R. Bringhurst, and P. Divieti
Role of calcium channels in carboxyl-terminal parathyroid hormone receptor signaling
Am J Physiol Cell Physiol, July 1, 2006; 291(1): C114 - C121.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online