Linked Life Data

15718388

Source:http://linkedlifedata.com/resource/pubmed/id/15718388

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2005-5-11
pubmed:abstractText
The syndrome of apparent mineralocorticoid excess (SAME) is an autosomal recessive form of salt-sensitive hypertension caused by deficiency of the kidney type 2 11beta-hydroxysteroid dehydrogenase (11betaHSD2). In this disorder, cortisol is not inactivated by 11betaHSD2, occupies mineralocorticoid receptors (MRs), and causes excessive sodium retention and hypertension. In renal medulla, prostaglandins derived from cyclooxygenase-2 (COX-2) stimulate sodium and water excretion, and renal medullary COX-2 expression increases after mineralocorticoid administration. We investigated whether medullary COX-2 also increases in rats with 11betaHSD2 inhibition and examined its possible role in the development of hypertension. 11betaHSD2 inhibition increased medullary and decreased cortical COX-2 expression in adult rats and induced high blood pressure in high-salt-treated rats. COX-2 inhibition had no effect on blood pressure in control animals but further increased blood pressure in high-salt-treated rats with 11betaHSD2 inhibition. COX-1 inhibition had no effect on blood pressure in either control or experimental animals. 11betaHSD2 inhibition also led to medullary COX-2 increase and cortical COX-2 decrease in weaning rats, primarily through activation of MRs. In the suckling rats, medullary COX-2 expression was very low, consistent with a urinary concentrating defect. 11betaHSD2 inhibition had no effect on either cortical or medullary COX-2 expression in the suckling rats, consistent with low levels of circulating corticosterone in these animals. These data indicate that COX-2 plays a modulating role in the development of hypertension due to 11betaHSD2 deficiency and that 11betaHSD2 regulates renal COX-2 expression by preventing glucocorticoid access to MRs during postnatal development.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0363-6119
pubmed:author
pubmed:issnType
Print
pubmed:volume
288
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
R1767-73
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:15718388-17-Hydroxysteroid Dehydrogenases, pubmed-meshheading:15718388-Animals, pubmed-meshheading:15718388-Animals, Newborn, pubmed-meshheading:15718388-Animals, Suckling, pubmed-meshheading:15718388-Blood Pressure, pubmed-meshheading:15718388-Cyclooxygenase 2, pubmed-meshheading:15718388-Enzyme Inhibitors, pubmed-meshheading:15718388-Female, pubmed-meshheading:15718388-Glycyrrhizic Acid, pubmed-meshheading:15718388-Hormone Antagonists, pubmed-meshheading:15718388-Hypertension, pubmed-meshheading:15718388-Immunoblotting, pubmed-meshheading:15718388-Immunohistochemistry, pubmed-meshheading:15718388-Kidney, pubmed-meshheading:15718388-Kidney Cortex, pubmed-meshheading:15718388-Kidney Medulla, pubmed-meshheading:15718388-Mifepristone, pubmed-meshheading:15718388-Pregnancy, pubmed-meshheading:15718388-Prostaglandin-Endoperoxide Synthases, pubmed-meshheading:15718388-Rats, pubmed-meshheading:15718388-Rats, Sprague-Dawley
pubmed:year
2005
pubmed:articleTitle
Interactions between 11beta-hydroxysteroid dehydrogenase and COX-2 in kidney.
pubmed:affiliation
George O'Brien Center for Kidney and Urologic Diseases and Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, TN 37232-4794, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural