Linked Life Data

12548089

Source:http://linkedlifedata.com/resource/pubmed/id/12548089

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2003-1-27
pubmed:abstractText
In the kidney, angiotensin-(1-7) [Ang-(1-7)] exhibits diuretic and natriuretic properties associated with an increase in prostaglandin production. The prohypertensive effects of Ang II are attenuated in rats infused with Ang-(1-7), consistent with recent work showing that Ang-(1-7) downregulates AT1 receptors in Chinese hamster ovary-AT1A or vascular smooth muscle cells. To determine whether exposure to Ang-(1-7) reduces AT1 receptors in the kidney through an increase in prostaglandin production, kidney slices from Sprague-Dawley rats were incubated with 10 n -1 microM Ang-(1-7) in the presence or absence of 5 microM meclofenamate, a cyclooxygenase inhibitor. Following these treatments, the kidney slices were retrieved, frozen, and sectioned for determination of [125I]-Ang II binding using in vitro receptor autoradiography. Greater than 90% of the specific binding was competed for by losartan, indicating that the majority of binding was to the AT1 receptor. Incubation of kidney slices with 1 microM Ang-(1-7) caused a 20% reduction in [125I]-Ang II binding (n = 8) in the cortical tubulointerstitium, which was prevented when Ang-(1-7)-treated slices were incubated in the presence of 5 microM meclofenamate (1 +/- 2% increase, n = 8; p < 0.05). Incubation with 5 microM meclofenamate alone had no effect on [125I]-Ang II binding (-3 +/- 3%). The decrease in [125I]-Ang II binding with Ang-(1-7) was also blocked by the Ang-(1-7) antagonist [d-Ala7]-Ang-(1-7). Treatment with 1 microM [d-Ala7]-Ang-(1-7) alone had no effect on [125I]-Ang II binding (-3 +/- 6% of control). Pretreatment with 1 microM Ang II caused a similar reduction in [125I]-Ang II binding in the cortical tubulointerstitium. Neither Ang-(1-7) nor Ang II had any effect on [125I]-Ang II binding in the glomeruli and the area of the vasa recta of the kidney. These original findings suggest that prior exposure to Ang-(1-7) or Ang II causes a modest decrease in the number of AT1 receptors in the cortical tubulointerstitial area of the kidney. The reduction in Ang II binding by Ang-(1-7) was blocked by meclofenamate and [d-Ala7]-Ang-(1-7), suggesting that cyclooxygenase products released through activation of a novel receptor participate in this effect.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0160-2446
pubmed:author
pubmed:issnType
Print
pubmed:volume
41
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
276-83
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Angiotensin-(1-7) reduces renal angiotensin II receptors through a cyclooxygenase-dependent mechanism.
pubmed:affiliation
The Hypertension and Vascular Disease Center, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157, U.S.A.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't