Enhanced expression of natriuretic peptide receptor A and B in neutrophils of culprit lesions in patients with acute myocardial infarction.

Natriuretic peptides and their specific receptors have been suggested to have regulatory effects on smooth muscle cell (SMC) growth and inflammatory cell reactions. However, the roles of natriuretic peptide receptor A (NPR‑A) and B (NPR‑B) in unstable plaques remain to be studied in detail. Frozen sections from 82 coronary artery segments were used. These segments were obtained at autopsy from 13 patients with acute myocardial infarction (AMI; 7 ruptured and 6 eroded plaques) and from 30 patients with non‑cardiovascular diseases. Antibodies against SMCs, endothelial cells, macrophages, neutrophils, NPR‑A, NPR‑B and neutral endopeptidase (NEP) were used. Neutrophil infiltration was identified in all lesions with plaque rupture or erosion. Double immunostaining identified that the majority of NPR‑A‑ or NPR‑B‑positive cells were neutrophils in ruptured and eroded plaques. Using morphometric analysis, no significant difference was observed in the percentage of NPR‑A‑ and NPR‑B‑positive cells between ruptured and eroded plaques, while the number of NEP‑positive neutrophils in ruptured plaques was significantly higher compared with eroded plaques (P<0.0001). These results of the distinct presence of NPR‑A‑ and NPR‑B‑positive cells in unstable plaques underlying AMI suggested that natriuretic peptides serve a role in regulating plaque instability in humans.

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