Charloux Anne, Chaouat Ari, Piquard François, Brandenberger Gabrielle, Weitzenblum Emmanuel, Geny Bernard
Institut de Physiologie, Service de Physiologie et d'Explorations Fonctionnelles et EA 3072, 4 rue Kirschleger, 67085 Strasbourg Cedex, France.
Peptides. 2006 Nov;27(11):2993-9. doi: 10.1016/j.peptides.2006.05.023. Epub 2006 Jul 5.
We examined the mechanisms of renal resistance to atrial and brain natriuretic peptides (ANP and BNP) in pulmonary hypertension (PH). Compared to eight controls, nine PH patients showed a reduced ability to excrete an acute sodium load despite increased circulating ANP, BNP and cyclic guanosine monophosphate (cGMP), their second messenger. Patients' reduced urinary cGMP/BNP and natriuresis/urinary cGMP ratios demonstrated impaired generation of and reduced renal response to cGMP, respectively. Therefore, PH patients hyporesponsiveness to cardiac natriuretic peptides is likely located both upstream and downstream cGMP generation. Natriuretic peptide signalling pathway disruptions might be accessible to therapy.
我们研究了肺动脉高压（PH）患者肾脏对心房钠尿肽和脑钠尿肽（ANP和BNP）产生抵抗的机制。与8名对照组相比，9名PH患者尽管循环中的ANP、BNP和环磷酸鸟苷（cGMP，它们的第二信使）水平升高，但排泄急性钠负荷的能力却降低。患者尿cGMP/BNP和利钠作用/尿cGMP比值降低，分别表明cGMP生成受损和肾脏对cGMP的反应减弱。因此，PH患者对心钠素反应低下可能存在于cGMP生成的上游和下游。利钠肽信号通路的破坏可能是可以治疗的。
