Source:http://linkedlifedata.com/resource/pubmed/id/21825222
Switch to
Predicate | Object |
---|---|
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
|