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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Mechanisms of renal hyporesponsiveness to BNP in heart failure
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Mechanisms of renal hyporesponsiveness to BNP in heart failure

机译：心力衰竭中肾对BNP的反应低下的机制

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摘要

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 could aid 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 in patients 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. Thus, a better understanding of renal hyporesponsiveness in HF is required to devise strategies to develop novel agents and technologies that directly restore renal BNP efficiency. It is hoped that development of these new therapeutic approaches will serve to limit sodium retention in patients with HF, which may ultimately delay the progression to overt HF.
机译：B型利钠肽（BNP）是血管活性肽家族的成员，是一种有效的利尿，利尿和血管舒张肽，有助于血压和体内稳态。这些特性使BNP成为理想的药物，可以帮助减轻肾功能差或恶化的体液过多患者。尽管BNP具有潜在的好处，但越来越多的证据表明，仅仅增加循环BNP的量并不一定会增加心力衰竭（HF）患者的利尿作用。此外，尽管BNP含量高，但当HF从补偿状态发展到失代偿状态时，利钠钠下降，表明出现了肾脏对BNP的耐药性。尽管可能是多因素的，但已经提出了几种机制来解释HF中的肾低反应性，包括但不限于肾BNP利用率降低，利钠肽受体下调以及BNP细胞内信号转导途径改变。因此，需要更好地了解心衰中的肾低反应性，以制定策略来开发可直接恢复肾BNP效率的新型药物和技术。希望这些新治疗方法的开发将有助于限制HF患者的钠retention留，这最终可能会延迟向明显HF的进展。

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