Response of Cardiac Mast Cells to Atrial Natriuretic Peptide.
From: Cell and Developmental Biology and Anatomy, School of Medicine, University of South Carolina, 6439 Garners Ferry Rd., Columbia, SC 29208, USA.
American journal of physiology. Heart and circulatory physiology
- Publish Date: Aug 2007
- ISSN: 0363-6135
- Volume: 293
- Issue: 2
- Pages: H1216-22
- Medium: Print
- Language: English
- Citation (JAMA): Murray David B, Gardner Jason D, Levick Scott P, et al. Response of Cardiac Mast Cells to Atrial Natriuretic Peptide.. Am. J. Physiol. Heart Circ. Physiol. Aug 2007;293:H1216-22
Abstract
Previously, our laboratory demonstrated that cardiac mast cell degranulation induces adverse ventricular remodeling in response to chronic volume overload. The purpose of this study was to investigate whether atrial natriuretic peptide (ANP), which is known to be elevated in chronic volume overload, 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. Infusion of ANP (225 pg/ml) into blood-perfused isolated rat hearts produced minimal activation of cardiac mast cells, similar to that seen in the control group. ANP also did not increase matrix metalloproteinase-2 activity, reduce collagen volume fraction, or alter diastolic or systolic cardiac function compared with 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 aortocaval fistula. Comparable increases of myocardial MMP-2 activity in treated and untreated rats with an aortocaval fistula were associated with equivalent decreases in ventricular collagen (P < 0.05 vs. sham-operated controls). Cardiac functional parameters and left ventricular hypertrophy were unaffected by anantin. 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.
Mesh Headings (Keywords): Animals, Aorta, Abdominal, Arteriovenous Fistula, Ascitic Fluid, Atrial Natriuretic Factor, Cell Degranulation, Collagen, Disease Models, Animal, Histamine Release, Hypertrophy, Left Ventricular, Male, Mast Cells, Matrix Metalloproteinase 2, Myocardium, Peptides, Cyclic, Rats, Rats, Sprague-Dawley, Vena Cava, Inferior, Ventricular Function, Left, Ventricular Remodeling
Check for Full Text / PubMed Unique Identifier (PMID): 17434981
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