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Vascular actions of brain natriuretic peptide: modulation by atherosclerosis and neutral endopeptidase inhibition

^a Cardiorenal Research Laboratory, Divisions of Cardiovascular Diseases and Cardiovascular Surgery, Departments of Internal Medicine, Physiology and Biochemistry and Molecular Biology, Mayo Clinic and Foundation, Rochester, Minnesota, USA

View larger version (23K): [in a new window]   Figure 1 Left, Bar graph showing BrdU uptake in optical density units as measured by colorimetry. *p < 0.05 vs. 0% FCS. p < 0.05 vs. 5% FCS. 0% FCS = BrdU uptake in cells not stimulated with FCS; 5% FCS = BrdU uptake in cells stimulated with 5% FCS; 5% FCS + BNP = BrdU uptake in cells coincubated in 5% FCS and BNP (10–7 mol/liter). Right, Bar graph showing cGMP generation. *p < 0.05 vs. control. p < 0.05 vs. 3 and 9 h. LOD = limit of detection.

View larger version (17K): [in a new window]   Figure 2 Left, Relaxation curves to BNP in the presence (open circles) and absence (open triangles) of endothelium in preconstricted aortic rings from normal rabbits. Right, Relaxation curves to BNP in the presence of endothelium in preconstricted aortic rings from normal rabbits (open circles), atherosclerotic rabbits (open triangles) and atherosclerotic rabbits treated for eight weeks with the orally active NEP inhibitor (NEPI), Candoxatril (UK 79300) (open diamonds). *p < 0.05 vs. normal. p < 0.05 vs. atherosclerosis.

View larger version (9K): [in a new window]   Figure 3 Bar graph showing atherosclerotic plaque area. CHOL = cholesterol-fed untreated rabbits (n = 6). NEPI = cholesterol-fed rabbits treated with Candoxatril (UK 79300) (n = 8). *p < 0.05 vs. cholesterol.