Ogawa Y, Itoh H, Nakao K
Department of Medicine, Kyoto University School of Medicine, Japan.
Clin Exp Pharmacol Physiol. 1995 Jan;22(1):49-53. doi: 10.1111/j.1440-1681.1995.tb01918.x.
The natriuretic peptide family consists of three endogenous ligands; atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and C-type natriuretic peptide (CNP), and is involved in the regulation of cardiovascular homeostasis. Both ANP and BNP act mainly as cardiac hormones and are produced predominantly by the atrium and ventricle, respectively. Expression of the BNP and ANP genes is greatly augmented in patients with congestive heart failure and animal models of ventricular hypertrophy or cardiomyopathy. In the heart, the BNP gene expression is regulated differently from the ANP gene expression both at transcriptional and post-transcriptional levels. Transgenic technology has provided the direct evidence that BNP as well as ANP is involved in the chronic blood pressure control. Contrasting with ANP and BNP, CNP does not act as a cardiac hormone but as a neuropeptide or an endothelium-derived autocrine/paracrine regulator. Endothelial production of CNP is remarkably augmented by various cytokines and growth factors such as transforming growth factor-beta and tumour necrosis factor-alpha, suggesting the pathophysiological significance of CNP in the process of various vascular disorders. Chromosomal mapping of natriuretic peptides has revealed that the CNP gene is localized on mouse chromosome 1, while ANP and BNP are tightly linked on mouse chromosome 4, suggesting that CNP, a local regulator, is functionally and evolutionarily distinct from ANP and BNP, both of which are cardiac hormones. Understanding the molecular biology and biochemistry of the natriuretic peptide family will lead to the better understanding of its physiological and pathophysiological implication, and the clinical application in cardiorenal regulation.
利钠肽家族由三种内源性配体组成，即心房利钠肽（ANP）、脑利钠肽（BNP）和C型利钠肽（CNP），参与心血管稳态的调节。ANP和BNP主要作为心脏激素起作用，分别主要由心房和心室产生。BNP和ANP基因的表达在充血性心力衰竭患者以及心室肥大或心肌病动物模型中显著增加。在心脏中，BNP基因表达在转录和转录后水平上与ANP基因表达的调控方式不同。转基因技术提供了直接证据，表明BNP以及ANP参与慢性血压控制。与ANP和BNP不同，CNP不作为心脏激素起作用，而是作为神经肽或内皮衍生的自分泌/旁分泌调节因子。各种细胞因子和生长因子，如转化生长因子-β和肿瘤坏死因子-α，可显著增加内皮细胞产生CNP，这表明CNP在各种血管疾病过程中的病理生理意义。利钠肽的染色体定位显示，CNP基因定位于小鼠1号染色体，而ANP和BNP在小鼠4号染色体上紧密连锁，这表明作为局部调节因子的CNP在功能和进化上与ANP和BNP不同，后两者均为心脏激素。了解利钠肽家族的分子生物学和生物化学将有助于更好地理解其生理和病理生理意义，以及在心脏肾脏调节中的临床应用。
