1974
DOI: 10.1007/bf01468936
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N-acetylation of p-amino-hippurate in kidneys with renal artery stenosis and in patients suffering from severe essential hypertension

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1978
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1979

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Cited by 3 publications
(3 citation statements)
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“…It is concluded that renal hypoxia per se is an unlikely cause for the reduced N-acetylation rate of PAH. Chronic hypoxia, however, may alter renal meta bolism by increasing the renal NEFA content which, in turn, inhibits the N-acetyltransferase activity.Recently, evidence has been presented that the renal metabolism of the clearance substance /i-aminohippurate (PAH) (cleavage of the glycin-group, N-acetylation) interferes with the reliability of the determination of the plasma flow [6][7][8]13], This is predominantly due to the different distribution of PAH and of its metabolites in urine and in plasma [13] and to the circumstance that Nacetylated metabolites (N-acetyl-PAH, N-acetyl-p-aminobenzoate) remain undetected by usual chemical analysis [6,13], Furthermore, the rate of N-acetylation of PAH varies largely, as was shown in rats with experimental hypertension and in humans suffering from severe essential hypertension or from renal artery stenosis [6.8.13]. ft was found significantly reduced in the clamped kidney of rats with two-kidney Goldblatt-hypertension (one renal artery clamped, both kidneys in situ), whereas the N-acetylation rate was normal in the contralateral organ [13].…”
mentioning
confidence: 99%
“…It is concluded that renal hypoxia per se is an unlikely cause for the reduced N-acetylation rate of PAH. Chronic hypoxia, however, may alter renal meta bolism by increasing the renal NEFA content which, in turn, inhibits the N-acetyltransferase activity.Recently, evidence has been presented that the renal metabolism of the clearance substance /i-aminohippurate (PAH) (cleavage of the glycin-group, N-acetylation) interferes with the reliability of the determination of the plasma flow [6][7][8]13], This is predominantly due to the different distribution of PAH and of its metabolites in urine and in plasma [13] and to the circumstance that Nacetylated metabolites (N-acetyl-PAH, N-acetyl-p-aminobenzoate) remain undetected by usual chemical analysis [6,13], Furthermore, the rate of N-acetylation of PAH varies largely, as was shown in rats with experimental hypertension and in humans suffering from severe essential hypertension or from renal artery stenosis [6.8.13]. ft was found significantly reduced in the clamped kidney of rats with two-kidney Goldblatt-hypertension (one renal artery clamped, both kidneys in situ), whereas the N-acetylation rate was normal in the contralateral organ [13].…”
mentioning
confidence: 99%
“…The difference between the calculated and the directly measured perfusion flow disappeared only when the PAH assay included all PAH metabolites. This implies that the validity of the C pah determination is influenced by an inconstant conversion rale of PAH as demon strated for the rat kidney in situ [18] and the human kidney [14,15].…”
Section: Discussionmentioning
confidence: 99%
“…I-hippuran has become a useful tool in kinetic investigations due to the ease of its analysis (Magnusson, 1962;Pritchard, et al, 1965;Blaufox, et al, 1963). human, rabbit, pig, guinea pig, mouse, cat, cattle, sheep, and rat (Malyusz, et al, 1979;Carpenter & Mudge, 1980;Smith, et al, 1945;Despopoulos, 1956;Frindt & Vial, 1968;Setchell & Blanch, 1961;Gyrd-Hansen & Rasmussen, 1970;Cross & Taggart, 1950;Girndt, et al, 1974a and1974b), but not in dogs (Mudge & Taggart, 1950b;Newman, et al, 1949). Of these reports, only Setchell and Blanch 1961 catheter at 1, 2, 4, 6, 15, 20, 25, 30, 40, 50, 60, 75, 90, 105, and 120…”
mentioning
confidence: 99%