Quantitative evaluation of pulomnary neuroendocrine cells and the role of nitric oxide in experimentally induced renovascular hypertension in male albino rats

ABSTRACT

Renovascular hypertension is the most common cause of secondary hypertension that leads to disorders in many systems and organs including the lung. The present work was carried out to determine how experimentally induced renovascular hypertension affects rat lung tissue with a special focus on the disorders in nitric oxide [NO] production as well as the number of pulmonary neuroendocrine cells. Twenty-one adult male albino rats were used; they were divided into three groups. Group I included five control rats, group II included eight rats that were sham operated, and group III included eight rats that were subjected to a renovascular hypertension procedure. Lower segments of the right lung lobes were obtained and then subjected to H and E and Masson's trichrome stains. Endothelial nitric oxide synthase [eNOS] and calcitonin antibody-2 were also used as immunohistochemical stains. Morphometric measurements included the area% of collagen fibers, the optical density of eNOS immunoreaction, and the number of calcitonin-positive neuroendocrine cells. Data were recorded and analyzed statistically. In group III, H and E-stained sections showed thickening of the tunica media of pulmonary arteries and alveolar walls with predominantly type II pneumocytes. Consequently, the thickened arteries showed a significant increase in the mean area% of collagen fibers, together with a significant decrease in the mean optical density of eNOS immunoreactivity when compared with the control group. The mean number of calcitonin immunoreactive neuroendocrine cells of group III showed a significant increase versus the control group. The current study showed an increased number of pulmonary neuroendocrine cells with renovascular hypertension. This increase may represent a compensatory mechanism to overcome renovascular hypertension. Thus, clinical trials could be conducted to prove the possible role of calcitonin-producing pulmonary neuroendocrine cells in controlling renovascular hypertension