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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1989-5-26
pubmed:abstractText
To examine the modulatory role of angiotensin II on the tubuloglomerular feedback (TGF) mechanism, TGF responses were assessed during control conditions, converting enzyme inhibition (CEI; MK 422, 0.6 mg/kg.hr) and during continued CEI with the replacement of angiotensin II. TGF responses were assessed from stop flow pressure (SFP) feedback responses obtained during step increases in the late proximal perfusion rate from 0-40 nl/min. SFP values in the absence of perfusion were used to estimate glomerular pressure (GP) under conditions where the influence of the TGF mechanism should be at a minimum. During CEI, the arterial pressure decreased from 124 +/- 3 to 106 +/- 3 mmHg and the estimated GP decreased from 53 +/- 1.4 to 49 +/- 0.8 mmHg. There was a marked attenuation in the magnitude of SFP feedback responses from 11.0 +/- 1.3 to 2.7 +/- 0.6 mmHg. TGF feedback responses, however, were restored towards normal during superimposed angiotensin II infusion (7.7 +/- 0.9 mmHg). These results indicate that converting enzyme inhibition decreases the effects of angiotensin II on the kidney through TGF dependent mechanism.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0255-6596
pubmed:author
pubmed:issnType
Print
pubmed:volume
12
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
180-5
pubmed:dateRevised
2008-2-26
pubmed:meshHeading
pubmed:year
1988
pubmed:articleTitle
Tubuloglomerular feedback-dependent influence of angiotensin II on the kidney in rats.
pubmed:affiliation
Department of Physiology and Biophysics, National Defense Medical Center, Taipei, Taiwan, Republic of China.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't