利钠肽受体-C可预防小鼠血管紧张素II介导的窦房结疾病。
Natriuretic Peptide Receptor-C Protects Against Angiotensin II-Mediated Sinoatrial Node Disease in Mice.
作者信息
Mackasey Martin, Egom Emmanuel E, Jansen Hailey J, Hua Rui, Moghtadaei Motahareh, Liu Yingjie, Kaur Jaspreet, McRae Megan D, Bogachev Oleg, Rafferty Sara A, Ray Gibanananda, Kirkby Adam W, Rose Robert A
机构信息
Department of Cardiac Sciences, Libin Cardiovascular Institute of Alberta, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada, and Department of Physiology and Pharmacology, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.
Department of Physiology and Biophysics, Faculty of Medicine, Dalhousie University, Halifax, Nova Scotia, Canada.
出版信息
JACC Basic Transl Sci. 2018 Dec 5;3(6):824-843. doi: 10.1016/j.jacbts.2018.08.004. eCollection 2018 Dec.
Sinoatrial node (SAN) disease mechanisms are poorly understood, and therapeutic options are limited. Natriuretic peptide(s) (NP) are cardioprotective hormones whose effects can be mediated partly by the NP receptor C (NPR-C). We investigated the role of NPR-C in angiotensin II (Ang II)-mediated SAN disease in mice. Ang II caused SAN disease due to impaired electrical activity in SAN myocytes and increased SAN fibrosis. Strikingly, Ang II treatment in NPR-C mice worsened SAN disease, whereas co-treatment of wild-type mice with Ang II and a selective NPR-C agonist (cANF) prevented SAN dysfunction. NPR-C may represent a new target to protect against the development of Ang II-induced SAN disease.
窦房结（SAN）疾病的发病机制尚不清楚，治疗选择也有限。利钠肽（NP）是具有心脏保护作用的激素，其作用部分可由NP受体C（NPR-C）介导。我们研究了NPR-C在小鼠血管紧张素II（Ang II）介导的窦房结疾病中的作用。Ang II由于窦房结心肌细胞电活动受损和窦房结纤维化增加而导致窦房结疾病。令人惊讶的是，在NPR-C基因敲除小鼠中进行Ang II治疗会使窦房结疾病恶化，而野生型小鼠联合使用Ang II和选择性NPR-C激动剂（cANF）可预防窦房结功能障碍。NPR-C可能是预防Ang II诱导的窦房结疾病发生的一个新靶点。
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