Linked Life Data

6183977

Source:http://linkedlifedata.com/resource/pubmed/id/6183977

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1983-1-27
pubmed:abstractText
The present study was performed to evaluate superficial nephron responses of the nonclipped kidney to angiotensin I converting enzyme inhibitor (CEI) (SQ 20,881, 3 mg . kg-1 . h-1) in two-kidney, one-clip Goldblatt hypertensive (GH) rats. Late proximal and early distal tubule collections were obtained before and during CEI. Significant increases in glomerular filtration rate, urine flow, sodium excretion, proximal and distal tubule flow rates, and single nephron glomerular filtration rate (from 24.6 +/- 1.7 to 27.5 +/- 1.6 nl/min) occurred despite reductions in arterial blood pressure (from 160 +/- 5 to 137 +/- 6 mmHg) during CEI. Proximal tubule absolute and fractional reabsorption of fluid, chloride, and total solute decreased significantly. In the nephron segment between the two collection sites, there were increases in absolute but decreases in fractional reabsorption. At the distal tubule level, fractional reabsorption but not absolute reabsorption decreased significantly. Proximal and distal tubule hydrostatic pressures increased significantly while peritubular capillary pressure decreased slightly. Responses following inhibition of angiotensin II formation suggest that there exists an angiotensin II-mediated enhancement in tubular reabsorption in the nonclipped kidney of Goldblatt hypertensive rats.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
243
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
F553-60
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1982
pubmed:articleTitle
Angiotensin-mediated alterations in nephron function in Goldblatt hypertensive rats.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.