Premium
A novel model for ischemic stroke ‐ the ANP gene disrupted (ANP−/−) mouse: molecular effects of hypertension in the development of stroke
Author(s) -
Ventura Nicole Marie,
Peterson Nichole T,
Tse M Yat,
Jin Albert Y,
Andrew R David,
Pang Stephen C
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.743.8
Subject(s) - atrial natriuretic peptide , stroke (engine) , medicine , brain natriuretic peptide , cardiology , left ventricular hypertrophy , angiotensin ii , endothelin receptor , muscle hypertrophy , myocardial infarction , heart failure , endocrinology , blood pressure , receptor , mechanical engineering , engineering
Cardiovascular disease (CVD) and stroke share many similar risk factors including hypertension. Alterations in the natriuretic peptide system (NPS) have shown to play a protective role in cardiac hypertrophy (CH) and myocardial infarction (MI). Given the similarities between CVD and stroke, these conditions may also share similar molecular mechanisms in their etiologies. The objective of this study is to develop a novel model for stroke using the chronically hypertensive, atrial natriuretic peptide (ANP) gene disrupted (ANP −/ − ) mouse to assess the effect of hypertension on stroke development. ANP +/− (salt‐sensitive) mice treated with either high (8%) or normal (0.8%) salt diet for 6 weeks were subjected to left middle cerebral artery occlusion (MCAO) for 30 min and allowed to recover for 24 hr. Results have demonstrated left ventricular (LV) hypertrophy and increased infarct volumes in mice treated with high dietary salt. Furthermore, we have characterized the alterations occurring in four major vasoactive systems in the brain; the NPS, the renin‐angiotensin system (RAS), the nitric oxide system (NOS) and endothelin system (ETS) using real‐time quantitative PCR (qPCR). Since ablation of ANP induces CH, understanding the molecular mechanisms of the above systems in the brain will allow us to assess if ANP plays a protective role for stroke as it does for MI. Support: HSFO and Canadian Foundation for Innovation. Grant Funding Source : Heart and Stroke Foundation of Ontario and Canadian Foundation for Innovation