Severe primary and secondary pulmonary arterial hypertension were associated with increased ACE immunostaining in the endothelium of intra-acinar peripheral pulmonary arteries compared to controls.
Case-Control (n=24)
Increased endothelial ACE expression in intra-acinar arteries of patients with primary and secondary pulmonary hypertension suggests local angiotensin II production may contribute to pulmonary vascular remodeling.
The hypothesis for this study was that increased local expression of vascular angiotensin-converting enzyme (ACE) may contribute to the arterial remodelling which accompanies pulmonary hypertension, since angiotensin II (ANG II) is an important mediator of pulmonary vascular cell growth. The expression of ACE was studied by immunohistochemistry in paraffin-embedded lung sections from adults undergoing heart-lung transplantation for severe primary (n=6) and secondary (n=7) pulmonary arterial hypertension (PH), compared with age-matched controls (n=11). An antigen retrieval technique was used prior to incubating sections with the anti-ACE monoclonal antibody, CG2, or the endothelial marker, monoclonal anti-CD31. In control lungs, the highest level of ACE immunostaining was seen in the alveolar capillary endothelium, with less intense staining in small intra-acinar pulmonary arteries and relatively little staining in larger preacinar arteries. ACE immunostaining was virtually absent in lymphatics and veins. In both primary and secondary PH, there was an increase in ACE immunostaining in the endothelium of intra-acinar peripheral pulmonary arteries compared with control lungs, extending to the level of alveolar ducts, as confirmed by semi-quantitative analysis. The increase in endothelial ACE expression in the intra-acinar arteries of patients with primary and secondary PH is consistent with the hypothesis that locally increased production of ANG II may contribute to the process of pulmonary vascular remodelling.
Orte et al. (Sat,) conducted a case-control in Severe primary and secondary pulmonary arterial hypertension (n=24). Severe primary and secondary pulmonary arterial hypertension vs. Age-matched controls was evaluated on ACE immunostaining in the endothelium of intra-acinar peripheral pulmonary arteries. Severe primary and secondary pulmonary arterial hypertension were associated with increased ACE immunostaining in the endothelium of intra-acinar peripheral pulmonary arteries compared to controls.