FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2014394353> ?p ?o ?g. }

• W2014394353 endingPage "1958" @default.
• W2014394353 startingPage "1949" @default.
• W2014394353 abstract "AT1 receptors mediate angiotensin II–induced release of nitric oxide in afferent arterioles.BackgroundRecent studies have indicated that angiotensin II (Ang II) possibly activates the nitric oxide (NO) system. We investigated the role of AT receptor subtypes (AT-R) in mediating the Ang II–induced NO release in afferent arterioles (Af) of mice.MethodsIsolated Af of mice were perfused, and the isotonic contraction measured. Further, NO release was determined using DAF-FM, a fluorescence indicator for NO. Moreover, we qualitatively assessed the expression of AT-R at the mRNA level using reverse transcription-polymerase chain reaction (RT-PCR).ResultsAng II reduced luminal diameters dose dependently (67.3 ± 6.3% at 10−6 mol/L). Inhibition of AT2-R with PD123.319 did not change the Ang II contractile response. AT1-R blockade with ZD7155 inhibited contraction. Stimulation of AT2-R during AT1-R inhibition with ZD7155, and preconstriction with norepinephrine (NE) had no influence on the diameter. Drug application via the perfusion pipette changed flow and pressure, and enhanced NO fluorescence by ΔF = 4.0 ± 0.4% (N = 14, background). Luminal application of Ang II (10−7 mol/L) increased the NO fluorescence by ΔF = 9.9 ± 1.2% (N = 8). AT1-R blockade blunted the increase to background levels (ΔF to 4.0 ± 0.3%, N = 6, P < 0.05), but AT2-R blockade did not (8.1 ± 0.9%, N = 9). L-NAME nearly abolished the Ang II effect on the NO fluorescence (ΔF = 1.6 ± 0.5% (N = 8). NE did not increase NO release beyond the background levels. RT-PCR showed expression of both AT1-R and AT2-R.ConclusionThe results indicate an Ang II–induced NO release in Af of mice, which is mediated by AT1-R. Thus, Ang II balances its own constrictor action in Af. This control mechanism is very important in view of high renin and angiotensin II concentration in the juxtaglomerular apparatus. AT1 receptors mediate angiotensin II–induced release of nitric oxide in afferent arterioles. Recent studies have indicated that angiotensin II (Ang II) possibly activates the nitric oxide (NO) system. We investigated the role of AT receptor subtypes (AT-R) in mediating the Ang II–induced NO release in afferent arterioles (Af) of mice. Isolated Af of mice were perfused, and the isotonic contraction measured. Further, NO release was determined using DAF-FM, a fluorescence indicator for NO. Moreover, we qualitatively assessed the expression of AT-R at the mRNA level using reverse transcription-polymerase chain reaction (RT-PCR). Ang II reduced luminal diameters dose dependently (67.3 ± 6.3% at 10−6 mol/L). Inhibition of AT2-R with PD123.319 did not change the Ang II contractile response. AT1-R blockade with ZD7155 inhibited contraction. Stimulation of AT2-R during AT1-R inhibition with ZD7155, and preconstriction with norepinephrine (NE) had no influence on the diameter. Drug application via the perfusion pipette changed flow and pressure, and enhanced NO fluorescence by ΔF = 4.0 ± 0.4% (N = 14, background). Luminal application of Ang II (10−7 mol/L) increased the NO fluorescence by ΔF = 9.9 ± 1.2% (N = 8). AT1-R blockade blunted the increase to background levels (ΔF to 4.0 ± 0.3%, N = 6, P < 0.05), but AT2-R blockade did not (8.1 ± 0.9%, N = 9). L-NAME nearly abolished the Ang II effect on the NO fluorescence (ΔF = 1.6 ± 0.5% (N = 8). NE did not increase NO release beyond the background levels. RT-PCR showed expression of both AT1-R and AT2-R. The results indicate an Ang II–induced NO release in Af of mice, which is mediated by AT1-R. Thus, Ang II balances its own constrictor action in Af. This control mechanism is very important in view of high renin and angiotensin II concentration in the juxtaglomerular apparatus." @default.
• W2014394353 created "2016-06-24" @default.
• W2014394353 creator A5059310123 @default.
• W2014394353 creator A5064176373 @default.
• W2014394353 creator A5076486841 @default.
• W2014394353 creator A5076981833 @default.
• W2014394353 creator A5082064420 @default.
• W2014394353 creator A5082447310 @default.
• W2014394353 date "2004-11-01" @default.
• W2014394353 modified "2023-10-15" @default.
• W2014394353 title "AT1 receptors mediate angiotensin II–induced release of nitric oxide in afferent arterioles" @default.
• W2014394353 cites W1772813204 @default.
• W2014394353 cites W1964047767 @default.
• W2014394353 cites W1967582620 @default.
• W2014394353 cites W1980182090 @default.
• W2014394353 cites W2002007414 @default.
• W2014394353 cites W2010055809 @default.
• W2014394353 cites W2026185220 @default.
• W2014394353 cites W2027605625 @default.
• W2014394353 cites W2037085464 @default.
• W2014394353 cites W2037425060 @default.
• W2014394353 cites W2039199937 @default.
• W2014394353 cites W2041839984 @default.
• W2014394353 cites W2047844782 @default.
• W2014394353 cites W2049940861 @default.
• W2014394353 cites W2051185167 @default.
• W2014394353 cites W2052037106 @default.
• W2014394353 cites W2063360581 @default.
• W2014394353 cites W2063391065 @default.
• W2014394353 cites W2064213110 @default.
• W2014394353 cites W2070707527 @default.
• W2014394353 cites W2075511108 @default.
• W2014394353 cites W2075974599 @default.
• W2014394353 cites W2079891784 @default.
• W2014394353 cites W2086239462 @default.
• W2014394353 cites W2086689607 @default.
• W2014394353 cites W2097489256 @default.
• W2014394353 cites W2101037152 @default.
• W2014394353 cites W2105300577 @default.
• W2014394353 cites W2108132405 @default.
• W2014394353 cites W2120428281 @default.
• W2014394353 cites W2131873159 @default.
• W2014394353 cites W2134319114 @default.
• W2014394353 cites W2142090351 @default.
• W2014394353 cites W2144826037 @default.
• W2014394353 cites W2146038402 @default.
• W2014394353 cites W2148888640 @default.
• W2014394353 cites W2155072308 @default.
• W2014394353 cites W2164732317 @default.
• W2014394353 cites W2187292204 @default.
• W2014394353 cites W2270877759 @default.
• W2014394353 cites W2315796856 @default.
• W2014394353 cites W2323127579 @default.
• W2014394353 doi "https://doi.org/10.1111/j.1523-1755.2004.00981.x" @default.
• W2014394353 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15496166" @default.
• W2014394353 hasPublicationYear "2004" @default.
• W2014394353 type Work @default.
• W2014394353 sameAs 2014394353 @default.
• W2014394353 citedByCount "90" @default.
• W2014394353 countsByYear W20143943532012 @default.
• W2014394353 countsByYear W20143943532013 @default.
• W2014394353 countsByYear W20143943532014 @default.
• W2014394353 countsByYear W20143943532015 @default.
• W2014394353 countsByYear W20143943532016 @default.
• W2014394353 countsByYear W20143943532017 @default.
• W2014394353 countsByYear W20143943532018 @default.
• W2014394353 countsByYear W20143943532019 @default.
• W2014394353 countsByYear W20143943532020 @default.
• W2014394353 countsByYear W20143943532021 @default.
• W2014394353 countsByYear W20143943532022 @default.
• W2014394353 countsByYear W20143943532023 @default.
• W2014394353 crossrefType "journal-article" @default.
• W2014394353 hasAuthorship W2014394353A5059310123 @default.
• W2014394353 hasAuthorship W2014394353A5064176373 @default.
• W2014394353 hasAuthorship W2014394353A5076486841 @default.
• W2014394353 hasAuthorship W2014394353A5076981833 @default.
• W2014394353 hasAuthorship W2014394353A5082064420 @default.
• W2014394353 hasAuthorship W2014394353A5082447310 @default.
• W2014394353 hasBestOaLocation W20143943531 @default.
• W2014394353 hasConcept C123915805 @default.
• W2014394353 hasConcept C126322002 @default.
• W2014394353 hasConcept C134018914 @default.
• W2014394353 hasConcept C163415756 @default.
• W2014394353 hasConcept C170493617 @default.
• W2014394353 hasConcept C185592680 @default.
• W2014394353 hasConcept C198710026 @default.
• W2014394353 hasConcept C24998067 @default.
• W2014394353 hasConcept C2780636983 @default.
• W2014394353 hasConcept C2908929049 @default.
• W2014394353 hasConcept C519581460 @default.
• W2014394353 hasConcept C71924100 @default.
• W2014394353 hasConcept C84393581 @default.
• W2014394353 hasConcept C86803240 @default.
• W2014394353 hasConceptScore W2014394353C123915805 @default.
• W2014394353 hasConceptScore W2014394353C126322002 @default.
• W2014394353 hasConceptScore W2014394353C134018914 @default.
• W2014394353 hasConceptScore W2014394353C163415756 @default.
• W2014394353 hasConceptScore W2014394353C170493617 @default.

• next