Mechanisms of renal hyporesponsiveness to BNP in heart failure

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00159816%3A_____%2F15%3A00062968" target="_blank" >RIV/00159816:_____/15:00062968 - isvavai.cz</a>

Výsledek na webu

<a href="http://dx.doi.org/10.1139/cjpp-2014-0356" target="_blank" >http://dx.doi.org/10.1139/cjpp-2014-0356</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1139/cjpp-2014-0356" target="_blank" >10.1139/cjpp-2014-0356</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Mechanisms of renal hyporesponsiveness to BNP in heart failure

Popis výsledku v původním jazyce

The B-type natriuretic peptide (BNP), a member of the family of vasoactive peptides, is a potent natriuretic, diuretic, and vasodilatory peptide that contributes to blood pressure and volume homeostasis. These attributes make BNP an ideal drug that couldaid in diuresing a fluid-overloaded patient who had poor or worsening renal function. Despite the potential benefits of BNP, accumulating evidence suggests that simply increasing the amount of circulating BNP does not necessarily increase natriuresis inpatients with heart failure (HF). Moreover, despite high BNP levels, natriuresis falls when HF progresses from a compensated to a decompensated state, suggesting the emergence of renal resistance to BNP. Although likely multifactorial, several mechanisms have been proposed to explain renal hyporesponsiveness in HF, including, but not limited to, decreased renal BNP availability, down-regulation of natriuretic peptide receptors, and altered BNP intracellular signal transduction pathways.

Název v anglickém jazyce

Mechanisms of renal hyporesponsiveness to BNP in heart failure

Popis výsledku anglicky

The B-type natriuretic peptide (BNP), a member of the family of vasoactive peptides, is a potent natriuretic, diuretic, and vasodilatory peptide that contributes to blood pressure and volume homeostasis. These attributes make BNP an ideal drug that couldaid in diuresing a fluid-overloaded patient who had poor or worsening renal function. Despite the potential benefits of BNP, accumulating evidence suggests that simply increasing the amount of circulating BNP does not necessarily increase natriuresis inpatients with heart failure (HF). Moreover, despite high BNP levels, natriuresis falls when HF progresses from a compensated to a decompensated state, suggesting the emergence of renal resistance to BNP. Although likely multifactorial, several mechanisms have been proposed to explain renal hyporesponsiveness in HF, including, but not limited to, decreased renal BNP availability, down-regulation of natriuretic peptide receptors, and altered BNP intracellular signal transduction pathways.

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

FR - Farmakologie a lékárnická chemie

OECD FORD obor

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Projekt

<a href="/cs/project/ED1.100%2F02%2F0123" target="_blank" >ED1.100/02/0123: Fakultní nemocnice u sv. Anny v Brně - Mezinárodní centrum klinického výzkumu (FNUSA - ICRC)</a><br>

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2015

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Canadian Journal of Physiology and Pharmacology

ISSN

0008-4212

e-ISSN

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Svazek periodika

93

Číslo periodika v rámci svazku

6

Stát vydavatele periodika

CA - Kanada

Počet stran výsledku

5

Strana od-do

399-403

Kód UT WoS článku

000355237100003

EID výsledku v databázi Scopus

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