Linked Life Data

3928683

Source:http://linkedlifedata.com/resource/pubmed/id/3928683

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1985-10-2
pubmed:abstractText
Despite great interest in the elevated circulating levels of calcitriol (1,25-[OH]2D) associated with the clinical syndrome of human primary hyperparathyroidism, the relative potencies of known and potential stimuli/suppressors of long-term calcitriol levels have not been evaluated in either clinical or experimentally induced hyperparathyroid states. Based on reports that aparathyroid animals exhibit suppressed plasma calcitriol concentration and that acute administration of parathyroid hormone (PTH) to both humans and experimental animals or to renal slices in vitro results in increased plasma calcitriol concentration/production rate, it might be predicted that a chronic experimental model of either hypercalcemic primary hyperparathyroidism or hypocalcemic secondary hyperparathyroidism would show increased plasma calcitriol concentration. Chronic alterations in plasma calcium concentration have not been implicated as modulating calcitriol levels in any species. Accordingly, we investigated the long-term response of plasma calcitriol concentration in states of sustained experimental primary and secondary hyperparathyroidism. Intact dogs (group I) undergoing continuous intravenous PTH infusion for 12 d developed sustained hypercalcemia and hypophosphatemia, and plasma calcitriol concentration decreased from 23 +/- 3 to 14 +/- 3 pg/ml (P less than 0.01). Subsequent chelator (EGTA)-induced chronic normalization of hypercalcemia during ongoing PTH infusion resulted in a large and sustained increase in plasma calcitriol concentration to supernormal levels, reversible during subsequent cessation of chelator infusion. In additional intact dogs (group II), chronic chelator-induced hypocalcemic secondary hyperparathyroidism resulted in a sustained increase in plasma calcitriol concentration despite hyperphosphatemia. In normal human subjects undergoing a 12-13-d continuous intravenous PTH infusion to result in sustained moderate hypercalcemia (12.0 +/- 0.2 mg/100 ml) and hypophosphatemia, plasma calcitriol concentration decreased significantly (P less than 0.01) as in group I dogs and was followed by reversal to normal levels in a recovery period. The present results provide strong evidence in both humans and dogs that during experimentally induced chronic PTH excess, alterations in plasma calcium concentration dictate the directional response of circulating calcitriol concentrations. The long-term potency of plasma calcium concentration as a modulator of calcitriol metabolism is sufficient to override opposing modulation by plasma phosphorus concentration and PTH.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/3928683-1188357, http://linkedlifedata.com/resource/pubmed/commentcorrection/3928683-14506, http://linkedlifedata.com/resource/pubmed/commentcorrection/3928683-206219, http://linkedlifedata.com/resource/pubmed/commentcorrection/3928683-209740, http://linkedlifedata.com/resource/pubmed/commentcorrection/3928683-236326, http://linkedlifedata.com/resource/pubmed/commentcorrection/3928683-34326, http://linkedlifedata.com/resource/pubmed/commentcorrection/3928683-420284, http://linkedlifedata.com/resource/pubmed/commentcorrection/3928683-4340153, http://linkedlifedata.com/resource/pubmed/commentcorrection/3928683-4373473, http://linkedlifedata.com/resource/pubmed/commentcorrection/3928683-5118156, http://linkedlifedata.com/resource/pubmed/commentcorrection/3928683-571872, http://linkedlifedata.com/resource/pubmed/commentcorrection/3928683-6101809, http://linkedlifedata.com/resource/pubmed/commentcorrection/3928683-6250405, http://linkedlifedata.com/resource/pubmed/commentcorrection/3928683-6255001, http://linkedlifedata.com/resource/pubmed/commentcorrection/3928683-6300178, http://linkedlifedata.com/resource/pubmed/commentcorrection/3928683-6320659, http://linkedlifedata.com/resource/pubmed/commentcorrection/3928683-6333430, http://linkedlifedata.com/resource/pubmed/commentcorrection/3928683-6546544, http://linkedlifedata.com/resource/pubmed/commentcorrection/3928683-6547151, http://linkedlifedata.com/resource/pubmed/commentcorrection/3928683-6749069, http://linkedlifedata.com/resource/pubmed/commentcorrection/3928683-6787928, http://linkedlifedata.com/resource/pubmed/commentcorrection/3928683-6892641, http://linkedlifedata.com/resource/pubmed/commentcorrection/3928683-6897931, http://linkedlifedata.com/resource/pubmed/commentcorrection/3928683-6992167, http://linkedlifedata.com/resource/pubmed/commentcorrection/3928683-7053991, http://linkedlifedata.com/resource/pubmed/commentcorrection/3928683-7121251, http://linkedlifedata.com/resource/pubmed/commentcorrection/3928683-7231553, http://linkedlifedata.com/resource/pubmed/commentcorrection/3928683-7351950, http://linkedlifedata.com/resource/pubmed/commentcorrection/3928683-885994, http://linkedlifedata.com/resource/pubmed/commentcorrection/3928683-91025
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0021-9738
pubmed:author
pubmed:issnType
Print
pubmed:volume
76
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
695-702
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1985
pubmed:articleTitle
Long-term control of plasma calcitriol concentration in dogs and humans. Dominant role of plasma calcium concentration in experimental hyperparathyroidism.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.