Linked Life Data

11270390

Source:http://linkedlifedata.com/resource/pubmed/id/11270390

Statements in which the resource exists.
SubjectPredicateObjectContext
pubmed-article:11270390rdf:typepubmed:Citationlld:pubmed
pubmed-article:11270390lifeskim:mentionsumls-concept:C0020538lld:lifeskim
pubmed-article:11270390lifeskim:mentionsumls-concept:C0206745lld:lifeskim
pubmed-article:11270390lifeskim:mentionsumls-concept:C0003018lld:lifeskim
pubmed-article:11270390lifeskim:mentionsumls-concept:C0914912lld:lifeskim
pubmed-article:11270390pubmed:issue3lld:pubmed
pubmed-article:11270390pubmed:dateCreated2001-3-27lld:pubmed
pubmed-article:11270390pubmed:abstractTextThe present study was performed to examine the role of endogenous bradykinin (BK) in the development of angiotensin II (Ang II)-induced hypertension in mice. BK B2receptor knockout (B2R-/-) and wild-type (B2R+/+) mice (22to 26 g) were infused with either saline (SAL) or Ang II (40ng/min) via an osmotic minipump implanted intraperitoneally. On day 12after implantation, there was no difference in systolic blood pressure (SBP, tail-cuff plethysmography) between SAL/B2R+/+ and SAL/B2R-/- mice(128+/-5 versus 133+/-6 mm Hg, n=24/group). In contrast, SBP was higher on day 12 of infusion in Ang II/B2R-/- than in Ang II/B2R+/+ mice (173+/-6versus 156+/-5 mm Hg; P<0.05, n=27 and 28). Mean arterial pressure (MAP)was also higher in anesthetized Ang II/B2R-/- mice than in Ang II/B2R+/+mice (139+/-3 versus 124+/-3 mm Hg; P<0.05, n=16 and 14). Unlike Ang II, long-term norepinephrine (NE) infusion via an osmotic minipump (45ng/min) caused equivalent increases in SBP in B2R+/+ and B2R-/- mice measured on day 12 after implantation (151+/-4 versus 149+/-5 mm Hg, n=9and 8). MAP also did not differ on day 13 after implantation between NE/B2R+/+ and NE/B2R-/- mice (120+/-6 versus 122+/-4 mm Hg, n=9 and 8). There were no differences in glomerular filtration rate and urinary sodium excretion among the groups. However, renal plasma flow (RPF) was lower in Ang II/B2R-/- mice than in Ang II/B2R+/+ mice (2.34+/-0.06 versus 4.33+/-0.19 mL x min-1 x g-1; P<0.05). Acute inhibition of NO synthase (NOS)with nitro-L-arginine-methyl ester (0.5 microg x g-1 x min-1) in SAL/B2+/+ and SAL/B2-/- mice caused equal increases in MAP (142+/-1 versus 145+/-1 mmHg) and decreases in RPF (2.06+/-0.06 versus 2.12+/-0.15 mL x min-1 x g-1).However, short-term NOS inhibition caused a greater increase in MAP of Ang II/B2R+/+ mice than of Ang II/B2R-/- mice, such that MAP after NOS inhibition in Ang II/B2R+/+ approached that of Ang II/B2R-/- mice (156+/-2versus 159+/-2 mm Hg). These changes were associated with a decrease in RPF in Ang II/B2R+/+ mice to values similar to those of Ang II/B2R-/- mice before NOS inhibition (2.12+/-0.09 versus 2.34+/-0.06 mL x min-1 x g-1). These results demonstrate that the kallikrein-kinin system selectively buffers the vasoconstrictor activity of Ang II. Furthermore, the enhanced susceptibility of B2R-/- mice to Ang II-induced hypertension and renal vasoconstriction is likely due to an impaired ability to release NO by endogenous kinins.lld:pubmed
pubmed-article:11270390pubmed:granthttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:11270390pubmed:granthttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:11270390pubmed:languageenglld:pubmed
pubmed-article:11270390pubmed:journalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:11270390pubmed:citationSubsetIMlld:pubmed
pubmed-article:11270390pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:11270390pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:11270390pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:11270390pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:11270390pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:11270390pubmed:statusMEDLINElld:pubmed
pubmed-article:11270390pubmed:monthMarlld:pubmed
pubmed-article:11270390pubmed:issn1524-4563lld:pubmed
pubmed-article:11270390pubmed:authorpubmed-author:HellerJJlld:pubmed
pubmed-article:11270390pubmed:authorpubmed-author:PINOD MDMlld:pubmed
pubmed-article:11270390pubmed:authorpubmed-author:KarasováLLlld:pubmed
pubmed-article:11270390pubmed:authorpubmed-author:VítkoSSlld:pubmed
pubmed-article:11270390pubmed:authorpubmed-author:HellerováSSlld:pubmed
pubmed-article:11270390pubmed:authorpubmed-author:CervenkaLLlld:pubmed
pubmed-article:11270390pubmed:authorpubmed-author:El-DahrS SSSlld:pubmed
pubmed-article:11270390pubmed:authorpubmed-author:SimováMMlld:pubmed
pubmed-article:11270390pubmed:issnTypeElectroniclld:pubmed
pubmed-article:11270390pubmed:volume37lld:pubmed
pubmed-article:11270390pubmed:ownerNLMlld:pubmed
pubmed-article:11270390pubmed:authorsCompleteYlld:pubmed
pubmed-article:11270390pubmed:pagination967-73lld:pubmed
pubmed-article:11270390pubmed:dateRevised2009-11-3lld:pubmed
pubmed-article:11270390pubmed:meshHeadingpubmed-meshheading:11270390...lld:pubmed
pubmed-article:11270390pubmed:meshHeadingpubmed-meshheading:11270390...lld:pubmed
pubmed-article:11270390pubmed:meshHeadingpubmed-meshheading:11270390...lld:pubmed
pubmed-article:11270390pubmed:meshHeadingpubmed-meshheading:11270390...lld:pubmed
pubmed-article:11270390pubmed:meshHeadingpubmed-meshheading:11270390...lld:pubmed
pubmed-article:11270390pubmed:meshHeadingpubmed-meshheading:11270390...lld:pubmed
pubmed-article:11270390pubmed:meshHeadingpubmed-meshheading:11270390...lld:pubmed
pubmed-article:11270390pubmed:meshHeadingpubmed-meshheading:11270390...lld:pubmed
pubmed-article:11270390pubmed:meshHeadingpubmed-meshheading:11270390...lld:pubmed
pubmed-article:11270390pubmed:meshHeadingpubmed-meshheading:11270390...lld:pubmed
pubmed-article:11270390pubmed:meshHeadingpubmed-meshheading:11270390...lld:pubmed
pubmed-article:11270390pubmed:meshHeadingpubmed-meshheading:11270390...lld:pubmed
pubmed-article:11270390pubmed:meshHeadingpubmed-meshheading:11270390...lld:pubmed
pubmed-article:11270390pubmed:meshHeadingpubmed-meshheading:11270390...lld:pubmed
pubmed-article:11270390pubmed:meshHeadingpubmed-meshheading:11270390...lld:pubmed
pubmed-article:11270390pubmed:meshHeadingpubmed-meshheading:11270390...lld:pubmed
pubmed-article:11270390pubmed:meshHeadingpubmed-meshheading:11270390...lld:pubmed
pubmed-article:11270390pubmed:year2001lld:pubmed
pubmed-article:11270390pubmed:articleTitleAngiotensin II-induced hypertension in bradykinin B2 receptor knockout mice.lld:pubmed
pubmed-article:11270390pubmed:affiliationDepartment of Experimental Medicine, Institute for Clinical and Experimental Medicine, 1958/9 Vídeská, 140 00 Prague 4, Czech Republic. luce@medicon.czlld:pubmed
pubmed-article:11270390pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:11270390pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
pubmed-article:11270390pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:11270390lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:11270390lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:11270390lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:11270390lld:pubmed