Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2011-9-15
pubmed:abstractText
Acute hypercalcemia inhibits plasma renin activity (PRA). How this occurs is unknown. We hypothesized that acute hypercalcemia inhibits PRA via the calcium-sensing receptor because of parathyroid hormone-mediated increases in renal cortical interstitial calcium via TRPV5. To test our hypothesis, acute in vivo protocols were run in sodium-restricted, anesthetized rats. TRPV5 messenger RNA expression was measured with real-time quantitative RT-PCR. Acute hypercalcemia significantly decreased PRA by 37% from 32.0±3.3 to 20.3±2.6 ng of angiotensin I per milliliter per hour (P<0.001). Acute hypercalcemia also significantly increased renal cortical interstitial calcium by 38% (1.73±0.06 mmol/L) compared with control values (1.25±0.05 mmol/L; P<0.001). PRA did not decrease in hypercalcemia in the presence of a calcium-sensing receptor antagonist, Ronacaleret (22.8±4.3 versus 21.6±3.6 ng of angiotensin I per milliliter per hour). Increasing plasma calcium did not decrease PRA in parathyroidectomized rats (22.5±2.6 versus 22.0±3.0 ng of angiotensin I per milliliter per hour). Parathyroidectomized rats were unable to increase their renal cortical interstitial calcium in response to hypercalcemia (1.01±0.11 mmol/L). Acutely replacing plasma parathyroid hormone levels did not modify the hypercalcemic inhibition of PRA in parathyroid-intact rats (39.1±10.9 versus 16.3±3.2 ng of angiotensin I per milliliter per hour; P<0.05). Renal cortical TRPV5 messenger RNA expression decreased by 67% in parathyroidectomized (P<0.001) compared with intact rats. Our data suggest that acute hypercalcemia inhibits PRA via the calcium-sensing receptor because of parathyroid hormone-mediated increases in renal cortical interstitial calcium via TRPV5.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin I, http://linkedlifedata.com/resource/pubmed/chemical/Calcium, http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels, http://linkedlifedata.com/resource/pubmed/chemical/Ecac1 protein, rat, http://linkedlifedata.com/resource/pubmed/chemical/Indans, http://linkedlifedata.com/resource/pubmed/chemical/Parathyroid Hormone, http://linkedlifedata.com/resource/pubmed/chemical/Phenylpropionates, http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Calcium-Sensing, http://linkedlifedata.com/resource/pubmed/chemical/Renin, http://linkedlifedata.com/resource/pubmed/chemical/TRPV Cation Channels, http://linkedlifedata.com/resource/pubmed/chemical/ronacaleret
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1524-4563
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
58
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
604-10
pubmed:meshHeading
pubmed-meshheading:21825222-Angiotensin I, pubmed-meshheading:21825222-Animals, pubmed-meshheading:21825222-Calcium, pubmed-meshheading:21825222-Calcium Channels, pubmed-meshheading:21825222-Hypercalcemia, pubmed-meshheading:21825222-Indans, pubmed-meshheading:21825222-Kidney, pubmed-meshheading:21825222-Male, pubmed-meshheading:21825222-Models, Animal, pubmed-meshheading:21825222-Parathyroid Hormone, pubmed-meshheading:21825222-Parathyroidectomy, pubmed-meshheading:21825222-Phenylpropionates, pubmed-meshheading:21825222-RNA, Messenger, pubmed-meshheading:21825222-Rats, pubmed-meshheading:21825222-Rats, Sprague-Dawley, pubmed-meshheading:21825222-Receptors, Calcium-Sensing, pubmed-meshheading:21825222-Renin, pubmed-meshheading:21825222-Signal Transduction, pubmed-meshheading:21825222-TRPV Cation Channels
pubmed:year
2011
pubmed:articleTitle
Hypercalcemia reduces plasma renin via parathyroid hormone, renal interstitial calcium, and the calcium-sensing receptor.
pubmed:affiliation
Hypertension and Vascular Research Division, Department of Internal Medicine, Henry Ford Hospital, Detroit, MI 48202, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural