Contributions to Nephrology 2004
DOI: 10.1159/000078713
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Novel Aspects of the Renal Renin-Angiotensin System: Angiotensin-(1-7),ACE2 and Blood Pressure Regulation

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Cited by 78 publications
(113 citation statements)
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“…The combination of physiologic and pharmacological approaches with molecular biology techniques has led to the identification of novel RAS components: Ang III, Ang IV and Ang-(1-7) (7,8,9); the Ang IV binding site insulin-regulated aminopeptidase (10); angiotensin-converting enzyme 2 (ACE2), an homologue of the "classic" angiotensin-converting enzyme (ACE) (11,12,13); and the Ang-(1-7) G protein-coupled receptor Mas (14). Among the novel RAS metabolites, Ang-(1-7) is particularly interesting.…”
Section: Hronic Renal Failure (Crf) In Childhood Frequently Resultsmentioning
confidence: 99%
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“…The combination of physiologic and pharmacological approaches with molecular biology techniques has led to the identification of novel RAS components: Ang III, Ang IV and Ang-(1-7) (7,8,9); the Ang IV binding site insulin-regulated aminopeptidase (10); angiotensin-converting enzyme 2 (ACE2), an homologue of the "classic" angiotensin-converting enzyme (ACE) (11,12,13); and the Ang-(1-7) G protein-coupled receptor Mas (14). Among the novel RAS metabolites, Ang-(1-7) is particularly interesting.…”
Section: Hronic Renal Failure (Crf) In Childhood Frequently Resultsmentioning
confidence: 99%
“…This heptapeptide is functionally linked to mechanisms that intrinsically regulate the function of the RAS (7,8,9,15). Ang-(1-7) is formed from Ang II by prolylendopeptidase, prolyl-carboxipeptidase or ACE2 (11,12,13) or directly from Ang I through hydrolysis by prolylendopeptidase and endopeptidase24.11 and metabolized by ACE to Ang-(1-5) (7,9). ACEi elevate Ang-(1-7) concentrations (16) by both increasing Ang I, the substrate for Ang-(1-7), as well as by preventing Ang-(1-7) degradation.…”
Section: Hronic Renal Failure (Crf) In Childhood Frequently Resultsmentioning
confidence: 99%
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“…Inhibition of ACE decreases Ang II production and increases Ang-(1-7) because of the following: (1) increased Ang-(1-7) formation from elevated levels of Ang I; and (2) inhibition of Ang-(1-7) metabolism by ACE. 19,42,[52][53][54][55][56] On the other hand, blockade of AT 1 receptors with its attendant elevation in both Ang I and Ang II stimulates ACE2 activity while facilitating an increase in Ang-(1-7) formation through the other Ang-(1-7)-forming enzymes. 20,48,49 …”
Section: Exploring the Significance Of The Ace Ace2 And Ang-(1-7) Axismentioning
confidence: 99%
“…In isolated, perfused rat kidneys and anesthetized animals [172,173], ANG-(1-7) has been shown to increase sodium and water excretion and the glomerular filtration rate (GFR) without affecting renovascular resistance. Hence, it is also possible that ANG-(1-7) induces diuresis and natriuresis by inhibiting renal tubular Na+/K+-ATPase [174,175]. However, ANG-(1-7) also induced antidiuresis in water-loaded rodents (258) and increased renal tubular sodium reabsorption in rats [176].…”
Section: Actions Of Ang-(1-7) In the Kidneymentioning
confidence: 99%