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Cardiac Tissue Sensitization to the Sympathetic Nervous System in Renal Ischemia/Reperfusion induced Cardiac Hypertrophy
Author(s) -
Panico Karine,
Alvim Juliana,
CarneiroRamos Marcela
Publication year - 2015
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.29.1_supplement.946.4
Subject(s) - kidney , medicine , endocrinology , renal ischemia , ischemia , sympathetic nervous system , homeostasis , renal function , propranolol , cardiac function curve , adrenergic , cardiology , receptor , reperfusion injury , blood pressure , heart failure
Objectives Heart and kidney share functions of the conservation of homeostasis. Acute kidney injury occurs by an abrupt decline in renal function and can lead to the development of cardiac hypertrophy (CH), among other ways, by catecholamines release into circulation. This study aims to investigate possible modulation of sympathetic nervous system (SNS) in CH development through the cardiac beta‐adrenergic receptors pathway in CH‐induced ischemic renal injury model. Methods C57BL/6 male mice (n=88) were subjected to surgical occlusion of left renal pedicle for 60min followed for reperfusion (REP) for 12 and 15 days. Another group of animals were treated with Propranolol (10 mg/kg/day) for 5 days after occlusion. Morphological and molecular parameters were used to evaluate kidney and CH status. Results Renal ischemia/reperfusion was able to induce CH after 12d. The left kidney mass was reduced (p<0.05) and an increase on Vimentin and urea levels were observed (p<0.001) and (p<0.05), respectively. Beta‐adrenergic receptors increased after 12days when compared to Sham group (p<0.05). Treatment with SNS inhibitor was able to improve the reduction of the left kidney mass. Conclusion CH was accompanied by an increase in levels of beta‐adrenergic receptor, suggesting an increase in cardiac sensitivity to SNS.