Woodard Geoffrey E, Rosado Juan A
National Institute of Allergy and Infectious Diseases, MSC 1876, Bethesda, Maryland 20892-1876, USA.
Int Rev Cell Mol Biol. 2008;268:59-93. doi: 10.1016/S1937-6448(08)00803-4.
Four major natriuretic peptides have been isolated: atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), C-type natriuretic peptide (CNP), and Dendroaspis-type natriuretic peptide (DNP). Natriuretic peptides play an important role in the regulation of cardiovascular homeostasis maintaining blood pressure and extracellular fluid volume. The classical endocrine effects of natriuretic peptides to modulate fluid and electrolyte balance and vascular smooth muscle tone are complemented by autocrine and paracrine actions that include regulation of coronary blood flow and, therefore, myocardial perfusion; modulation of proliferative responses during myocardial and vascular remodeling; and cytoprotective anti-ischemic effects. The actions of natriuretic peptides are mediated by the specific binding of these peptides to three cell surface receptors: type A natriuretic peptide receptor (NPR-A), type B natriuretic peptide receptor (NPR-B), and type C natriuretic peptide receptor (NPR-C). NPR-A and NPR-B are guanylyl cyclase receptors that increase intracellular cGMP concentration and activate cGMP-dependent protein kinases. NPR-C has been presented as a clearance receptor and its activation also results in inhibition of adenylyl cyclase activity. The wide range of effects of natriuretic peptides might be the base for the development of new therapeutic strategies of great benefit in patients with cardiovascular problems including coronary artery disease or heart failure. This review summarizes current literature concerning natriuretic peptides, their receptors and their effects on fluid/electrolyte balance, and vascular and cardiac physiology and pathology, including primary hypertension and myocardial infarction. In addition, we will attempt to provide an update on important issues regarding natriuretic peptides in congestive heart failure.
心房利钠肽（ANP）、脑利钠肽（BNP）、C型利钠肽（CNP）和树眼镜蛇型利钠肽（DNP）。利钠肽在调节心血管稳态、维持血压和细胞外液容量方面发挥着重要作用。利钠肽调节液体和电解质平衡以及血管平滑肌张力的经典内分泌作用，还得到了自分泌和旁分泌作用的补充，这些作用包括调节冠状动脉血流量，进而调节心肌灌注；调节心肌和血管重塑过程中的增殖反应；以及细胞保护抗缺血作用。利钠肽的作用是通过这些肽与三种细胞表面受体的特异性结合来介导的：A型利钠肽受体（NPR-A）、B型利钠肽受体（NPR-B）和C型利钠肽受体（NPR-C）。NPR-A和NPR-B是鸟苷酸环化酶受体，可增加细胞内cGMP浓度并激活cGMP依赖性蛋白激酶。NPR-C被认为是一种清除受体，其激活也会导致腺苷酸环化酶活性受到抑制。利钠肽的广泛作用可能是开发对包括冠状动脉疾病或心力衰竭在内的心血管问题患者大有裨益的新治疗策略的基础。本综述总结了有关利钠肽、其受体及其对液体/电解质平衡、血管和心脏生理及病理（包括原发性高血压和心肌梗死）影响的当前文献。此外，我们将尝试提供关于充血性心力衰竭中利钠肽重要问题的最新信息。
