Abstract

Overweight is associated with triglyceride accumulation in cardiomyocytes, which can cause cardiac dysfunction. It is also associated with reduced synthesis and plasma concentration of atrial natriuretic peptide (ANP). In adipocytes, ANP stimulates lipolysis through natriuretic peptide receptor-A (NPR-A), leading to cGMP-dependent phosphorylation of hormone-sensitive lipase. Cardiac myocytes express NPR-A and hormone-sensitive lipase. In the present study, we investigated whether ANP affects triglyceride stores in the heart. Subcutaneously implanted osmotic minipumps were used to administer ANP (125 or 500 ng/kg/min) or saline to obese leptin-deficient (ob/ob) mice or lean control mice (ob/+ ) for a week. ANP (500 ng/kg/min) reduced blood pressure but did not affect the cardiac triglyceride stores or mRNA expression of NPR-A and NPR-C. Also, deficiency of NPR-A did not affect the cardiac triglyceride content. Finally, addition of ANP to the culture medium (10-7 mol/l) increased cellular cGMP content (P = 0.009) but did not affect triglyceride stores in HL-1 cardiac myocyte cultures. Hence, ANP does not affect triglyceride stores in the murine heart.

Original languageEnglish
JournalCardiovascular Endocrinology
Volume3
Issue number3
Pages (from-to)92-7
Number of pages6
ISSN2162-6898
DOIs
Publication statusPublished - Sept 2014

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