Degradation of porcine brain natriuretic peptide (pBNP-26) by endoprotease-24.11 from kidney cortical membranes

Vogt‐Schaden, Marlies; Gagelmann, M.; Hock, D.; Herbst, F.; Forssmann, Wolf‐Georg

doi:10.1016/0006-291x(89)91366-1

Cited by 23 publications

(15 citation statements)

References 26 publications

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“…It has also been observed that the amino-terminal region of the peptides plays an important role in the susceptibility to hydrolysis by NEP. Vogt-Schaden et al (25 ) observed that the Cys-Phe bond in human ANP, but not the corresponding Cys-Phe bond in porcine BNP, was cleaved by NEP, and they related this observation to the difference in the amino termini of the peptides. In our experiments, we found clear NEP-mediated degradation of ANP (1-28).…”

Section: Discussionmentioning

confidence: 99%

Dipeptidyl-Peptidase IV Converts Intact B-Type Natriuretic Peptide into Its des-SerPro Form

et al. 2006

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Section: Discussionmentioning

confidence: 99%

Dipeptidyl-Peptidase IV Converts Intact B-Type Natriuretic Peptide into Its des-SerPro Form

et al. 2006

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“…Several authors have shown that BNP is a substrate for E-24.11 in vitro (Vogt-Schaden et al, 1989;Norman et al, 1991). The site of hydrolysis of BNP differs from that for ANP and, like the molecular form, varies between species.…”

Section: Discussionmentioning

confidence: 99%

Effect of endopeptidase‐24.11 inhibition and of atrial natriuretic peptide clearance receptor ligand on the response to rat brain natriuretic peptide in the conscious rat

Kirk¹,

Wilkins²

1993

British J Pharmacology

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1 The present studies examined the effect of (a) a specific endopeptidase-24.11 (E-24.11) inhibitor (candoxatrilat) and (b) a ligand for the atrial natriuretic peptide (ANP) clearance receptor (SC 46542) on the renal and blood pressure response to brain natriuretic peptide (BNP) in conscious rats.2 Infusion of BNP 200 ng kg-' min-' for 60 min produced a small rise in urinary sodium and guanosine 3':5'-cyclic monophosphate (cyclic GMP) excretion with a non-significant fall in mean arterial blood pressure. 3 Candoxatrilat (3 mg kg-') alone had no significant effect on sodium excretion or blood pressure but markedly potentiated the natriuretic response to BNP.4 Similarly SC 46542 ( 68 fig kg-'; 6.8 fig kg-' min-') which produced no significant effect on its own, potentiated the natriuresis-induced by BNP, although the effect was of shorter duration compared to that of candoxatrilat. 5 The data indicate two approaches to the potentiation of the renal activity of BNP and suggest that BNP may mediate some of the activity of E-24.11 inhibitors reported in cardiac failure.

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“…Third, binding to the ANP receptor [16] may be another metabolic pathway of BNP. Finally, decreased cardiac function in HD patients may be accompanied by elevated plasma BNP levels.…”

Section: Discussionmentioning

confidence: 99%

Plasma Concentration of Brain Natriuretic Peptide as an Indicator of Cardiac Ventricular Function in Patients on Hemodialysis

Nitta¹,

Kawashima²,

Yumura³

et al. 1998

Am J Nephrol

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The plasma concentration of human brain natriuretic peptide (BNP) was measured by immunoradiometric assay in patients on maintenance hemodialysis (HD) to assess the possible relationship between the plasma levels of this peptide and cardiac ventricular function, as judged by M-mode echocardiography. The plasma BNP levels in the pre-HD state were significantly higher (688.5 ± 154.5 pg/ml) than those of healthy subjects (<40 pg/ml). In addition, the plasma BNP levels were slightly decreased during HD (post-HD, 617.3 ± 157.1 pg/ml). There was no correlation between the plasma levels of BNP and body weight changes during HD. The mean plasma BNP level was significantly higher in the group of patients with a low left ventricular ejection fraction (EF < 60%) than in the group with a normal EF. In the patients as a whole, there was an inverse correlation between plasma BNP levels and EF. Moreover, a positive correlation was found between plasma BNP levels and left ventricular mass index (r = 0.57, p < 0.05). These results suggest that plasma BNP levels increase in response to chronic stimulation in accordance with increased cardiac load, and that they may be a possible indicator of reduced ventricular function in HD patients.

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Degradation of porcine brain natriuretic peptide (pBNP-26) by endoprotease-24.11 from kidney cortical membranes

Cited by 23 publications

References 26 publications

Dipeptidyl-Peptidase IV Converts Intact B-Type Natriuretic Peptide into Its des-SerPro Form

Dipeptidyl-Peptidase IV Converts Intact B-Type Natriuretic Peptide into Its des-SerPro Form

Effect of endopeptidase‐24.11 inhibition and of atrial natriuretic peptide clearance receptor ligand on the response to rat brain natriuretic peptide in the conscious rat

Plasma Concentration of Brain Natriuretic Peptide as an Indicator of Cardiac Ventricular Function in Patients on Hemodialysis

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