title: The secretion patterns and roles of cardiac and circulating arginine vasopressin during the development of heart failure.
abstract: OBJECTIVE
  The aim of this study is to investigate local cardiac and circulating AVP secretion during heart failure and to determine whether AVP mediates ventricular remodeling.
  
  
  METHODS
  We assessed cardiac function and AVP levels of post-myocardial infarction (MI) heart-failure rats 3 weeks (n = 10), 4 weeks (n = 10), 6 weeks (n = 10), 9 weeks (n = 15) after the proximal left anterior descending coronary artery (LAD) ligation. Ten sham-operated rats were used as the control group. In vitro, cardiac microvascular endothelial cells (CMECs) were initiated from isolated Wistar rat hearts and subjected to Ang II to induce AVP expression and secretion. Besides, the effects of AVP stimulation on CMECs and cardiac fibroblasts (CFs) were studied using methylthiazol tetrazolium assay, Western blotting and real-time PCR.
  
  
  RESULTS
  With cardiac dysfunction, plasma and local cardiac AVP, aldosterone levels increased over time, peaking at 9 weeks post-MI. AVP levels were negatively correlated with serum Na(+) and LVEF but positively correlated with LVEDD and myocardial hydroxyproline. In CMECs treated with Ang II, AVP mRNA and protein expression increased. In addition, AVP promoted CFs proliferation and up-regulated the expression of endothelin-1 and connective tissue growth factor.
  
  
  CONCLUSIONS
  CMECs are the cellular sources of elevated local heart AVP stimulated with Ang II/AT1. An intrinsic cardiac AVP system exists. Local cardiac and circulating AVP secretion were enhanced by deteriorating cardiac function. AVP may promote ventricular remodeling. Thus, AVP could be an important mediator of myocardial fibrosis in late-stage heart failure.
authors.affiliation: Department of Cardiology, First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510080, China.
authors.forename: Xuanlan
authors.initials: X
authors.lastname: Chen
authors.affiliation: Department of Cardiology, First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510080, China.
authors.forename: Guihua
authors.initials: G
authors.lastname: Lu
authors.affiliation: Department of Cardiology, First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510080, China.
authors.forename: Kaiyu
authors.initials: K
authors.lastname: Tang
authors.affiliation: Department of Cardiology, First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510080, China.
authors.forename: Qinglang
authors.initials: Q
authors.lastname: Li
authors.affiliation: Department of Cardiology, First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510080, China. Electronic address: xiurengao@163.com.
authors.forename: Xiuren
authors.initials: X
authors.lastname: Gao
mesh_terms: D000450:Aldosterone / Q000097:blood; D000818:Animals; D001127:Arginine Vasopressin / Q000097:blood / Q000378:metabolism*; D004195:Disease Models, Animal; D006333:Heart Failure / Q000097:blood / Q000378:metabolism*; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D020257:Ventricular Remodeling / Q000502:physiology*
chemical_list: D001127:Arginine Vasopressin; D000450:Aldosterone
keywords: Aldosterone; Arginine vasopressin; Cardiac microvascular endothelial cells; Heart failure; Myocardial fibrosis