Linked Life Data

2943240

Source:http://linkedlifedata.com/resource/pubmed/id/2943240

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1986-9-16
pubmed:abstractText
To characterize the decrease in glomerular permeability that occurs in contralateral kidney of renovascular hypertension, glomerular hemodynamics were studied in Goldblatt hypertensive and normotensive control rats. The effects of converting enzyme inhibition (captopril) and renal vasodilatation induced with hyperoncotic plasma were evaluated: in addition, glomerular morphometry was performed. In hypertension, glomerular capillary pressure was increased, ultrafiltration coefficient was decreased, single-nephron filtration rate was normal and afferent resistance was elevated. Captopril rose glomerular filtration rate only in normotensive rats, but ultrafiltration coefficient increased in both groups. Hyperoncotic plasma induced a 98% increment in filtration rate and ultrafiltration coefficient rose by 48% in normotensive group. In hypertensive rats, filtration rate increased only 15% and ultrafiltration coefficient diminished 6%, morphometric studies showed dilatation of capillary loops and a larger glomerular volume. Similar response to captopril in both groups of rats suggest that the reduction in ultrafiltration coefficient in hypertension is not dependent of angiotensin; lack of response to hyperoncotic plasma suggests that it could be produced by structural changes in capillary wall that diminish hydraulic permeability since the larger glomerular volume indicates a greater area for filtration.
pubmed:language
spa
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0020-3785
pubmed:author
pubmed:issnType
Print
pubmed:volume
56
pubmed:owner
NLM
pubmed:authorsComplete
N
pubmed:pagination
13-24
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:articleTitle
[A change in glomerular permeability in renovascular hypertension. Participation of angiotensin and structural lesions].
pubmed:publicationType
Journal Article, English Abstract