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1 Cell & Developmental Biology & Anatomy, University of South Carolina School of Medicine, Columbia, South Carolina, United States
2 Cell and Developmental Biology and Anatomy, University of South Carolina, Columbia, South Carolina, United States; Cell & Developmental Biology & Anatomy, University of South Carolina School of Medicine, Columbia, South Carolina, United States
3 Cell and Developmental Biology and Anatomy, University of South Carolina, Columbia, South Carolina, United States
4 Cell and Developmental Biology & Anatomy, University of South Carolina, Columbia, South Carolina, United States
5 University of South Carolina, South Carolina, United States
* To whom correspondence should be addressed. E-mail: jjanicki{at}gw.med.sc.edu.
Previously our laboratory has demonstrated that cardiac mast cell degranulation induces adverse ventricular remodeling in response to chronic volume overload (CVO). The purpose of this study was to investigate whether atrial natriuretic peptide (ANP), which is known to be elevated in CVO, causes cardiac mast cell degranulation. Relative to control, ANP induced significant histamine release from peritoneal mast cells, whereas isolated cardiac mast cells were not responsive. Likewise, infusion of 225 pg/ml of ANP in blood perfused isolated rat hearts produced minimal activation of cardiac mast cells that was similar to that in the control group. ANP also did not increase in MMP-2 activity or cause a reduction in collagen volume fraction, and did not alter diastolic or systolic cardiac function, relative to saline-treated controls. In a subsequent study to evaluate the effects of natriuretic peptide receptor antagonism on volume overload induced ventricular remodeling; Anantin was administered to rats with an aorto-caval fistula. Both untreated and treated groups had comparable increases in myocardial MMP-2 activity post fistula, which were associated with equivalent decreases in ventricular collagen (p<0.05 versus sham-operated controls). Cardiac functional parameters and LV hypertrophy were unaffected by Anantin treatment. We conclude that ANP is not a cardiac mast cell secretagogue and is not responsible for the cardiac mast cell-mediated adverse ventricular remodeling in response to volume overload.
This article has been cited by other articles:
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  D. B. Murray, R. McMillan, G. L. Brower, and J. S. Janicki ETA selective receptor antagonism prevents ventricular remodeling in volume-overloaded rats Am J Physiol Heart Circ Physiol, July 1, 2009; 297(1): H109 - H116. [Abstract] [Full Text] [PDF]
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D. B. Murray, J. D. Gardner, G. L. Brower, and J. S. Janicki Effects of nonselective endothelin-1 receptor antagonism on cardiac mast cell-mediated ventricular remodeling in rats Am J Physiol Heart Circ Physiol, March 1, 2008; 294(3): H1251 - H1257. [Abstract] [Full Text] [PDF]
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