Abstract:
UNLABELLED:Inhibition of pressure natriuresis in mice lacking the AT2 receptor. BACKGROUND:Angiotensin II type 2 (AT2) receptor knockout mice have higher blood pressures than wild-type mice; however, the hypertension is imperfectly defined. We tested the hypothesis that renal mechanisms could be contributory. METHODS:We conducted pressure-natriuresis-diuresis experiments, measured renal cortical and medullary blood flow by laser Doppler methods, and explored cytochrome P450-dependent arachidonic acid metabolism by means of reverse transcription-polymerase chain reaction. RESULTS:Blood pressure was 15 mm Hg higher in AT2 receptor knockout mice than in controls, and pressure diuresis and natriuresis curves were shifted rightward. At similar renal perfusion pressures (113 to 118 mm Hg), wild-type mice excreted threefold more sodium and water than AT2 receptor knockout mice. Fractional sodium and water excretion curves were shifted rightward in parallel. Renal blood flow ranged between 6.72 and 7.88 mL/min/g kidney wet weight (kwt) in wild-type and between 5.84 and 6.15 mL/min/g kwt in AT2 receptor knockout mice. Renal vascular resistance was increased in AT2A receptor knockout mice. Cortical blood flow readings leveled at 2.5 V in wild-type and 1.5 V in AT2 receptor knockout mice. Medullary blood flow readings ranged between 0.8 and 1.0 V and increased 116% in wild-type mice as renal perfusion pressure was increased. This increase did not occur in AT2 receptor knockout mice. The glomerular filtration rate (GFR) was similar in both groups at approximately 1 mL/min/g kwt. Renal microsomes from AT2 receptor knockout mice had less activity in hydroxylating arachidonic acid to 20-hydroxyeicosatetraenoic acid (20-meter) than controls, whereas renal AT1 receptor gene expression was increased in AT2 receptor knockout mice. CONCLUSIONS:Hemodynamic and tubular factors modify renal sodium handling in AT2 receptor knockout mice and may cause hypertension. AT2 receptor disruption induces alterations of other regulatory systems, including altered arachidonic acid metabolism, that may contribute to the intrarenal differences observed between AT2 receptor knockout and wild-type mice.
journal_name
Kidney Intjournal_title
Kidney internationalauthors
Gross V,Schunck WH,Honeck H,Milia AF,Kärgel E,Walther T,Bader M,Inagami T,Schneider W,Luft FCdoi
10.1046/j.1523-1755.2000.00820.xsubject
Has Abstractpub_date
2000-01-01 00:00:00pages
191-202issue
1eissn
0085-2538issn
1523-1755pii
S0085-2538(15)46718-3journal_volume
57pub_type
杂志文章abstract::We examined the role of the plasminogen activator/plasmin system in extracellular matrix (ECM) degradation by human mesangial cells cultured on thin films of 125I-labeled ECM (Matrigel). ECM degradation (release of 125I into the medium) was dependent on exogenous plasminogen, proportional to the number of mesangial ce...
journal_title:Kidney international
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journal_title:Kidney international
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journal_title:Kidney international
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journal_title:Kidney international
pub_type: 杂志文章,评审
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journal_title:Kidney international
pub_type: 杂志文章
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pub_type: 杂志文章
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pub_type: 评论,杂志文章
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