Linked Life Data

9892161

Source:http://linkedlifedata.com/resource/pubmed/id/9892161

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1999-3-11
pubmed:abstractText
Renin secretion from isolated, perfused, thick ascending limb/glomerulus preparations from mice, under baseline conditions, has been found to be approximately 10-fold higher than that observed with the same preparations from rabbits. Higher renin secretion rates appear to be accompanied by higher plasma renin activities in mice, compared with rats, rabbits, or humans. Experiments were performed to determine the extent of the renin-angiotensin system dependence of renal hemodynamics in mice. Administration of the type 1 angiotensin II (AT1) receptor blocker candesartan (10 mg/kg) to untreated control mice increased renal blood flow by 55% (from 1.8+/-0.2 to 2.8+/-0.2 ml/min) and decreased renal vascular resistance by 42% (from 55+/-7.5 to 31.8+/-2.3 mmHg x min/ml). Similarly, acute extracellular volume expansion increased renal blood flow by 84% and reduced renal vascular resistance by 48%. In mice with null mutations in either the AT1 receptor or the angiotensin-converting enzyme gene, renal vascular resistance was significantly lower than in wild-type mice. Tubuloglomerular feedback, which is an angiotensin II-dependent vasoconstrictor response, was found to be abolished in both strains of knockout mice. Acute AT1 receptor blockade by candesartan reduced tubuloglomerular feedback responses to a flow rate step change of 0 to 30 nl/min by approximately 80% (from 6.1+/-1.4 to 1.3+/-0.4 mmHg). Candesartan increased the steady-state autoregulatory index from 0.19 to 0.55 (in a pressure interval of 90 to 100 mmHg), suggesting reduced efficiency of steady-state autoregulation. These results indicate that the renin-angiotensin system exerts tonic control over renal vascular resistance in mice to a greater extent than previously observed in other mammalian species.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1046-6673
pubmed:author
pubmed:issnType
Print
pubmed:volume
10 Suppl 11
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
S184-8
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:9892161-Angiotensin Receptor Antagonists, pubmed-meshheading:9892161-Animals, pubmed-meshheading:9892161-Benzimidazoles, pubmed-meshheading:9892161-Glomerular Filtration Rate, pubmed-meshheading:9892161-Hemodynamics, pubmed-meshheading:9892161-Homeostasis, pubmed-meshheading:9892161-Kidney Glomerulus, pubmed-meshheading:9892161-Male, pubmed-meshheading:9892161-Mice, pubmed-meshheading:9892161-Mice, Knockout, pubmed-meshheading:9892161-Mutation, pubmed-meshheading:9892161-Peptidyl-Dipeptidase A, pubmed-meshheading:9892161-Receptor, Angiotensin, Type 1, pubmed-meshheading:9892161-Receptor, Angiotensin, Type 2, pubmed-meshheading:9892161-Receptors, Angiotensin, pubmed-meshheading:9892161-Renin, pubmed-meshheading:9892161-Renin-Angiotensin System, pubmed-meshheading:9892161-Tetrazoles, pubmed-meshheading:9892161-Vascular Resistance
pubmed:year
1999
pubmed:articleTitle
Renin-angiotensin system dependence of renal hemodynamics in mice.
pubmed:affiliation
Department of Physiology, The University of Michigan, Ann Arbor, USA.
pubmed:publicationType
Journal Article, Comparative Study, In Vitro, Research Support, U.S. Gov't, P.H.S.