Corpo carotídeo e hipertensão: alterações celulares e da matriz extracelular

Abstract

The increased cardiovascular disease as the key features and, more common, increasing blood pressure (BP). This can cause complications in other organs and cause various diseases and may lead to death. Hypertension is a multifactorial syndrome, whose incidence is higher in obese, sedentary and consumers in excess alcohol and salt. The carotid body (CC) is a chemoreceptor organ located in bifurcation carotid artery, consisting of basic structures called carotid glomus. Each is made up of carotid glomus type 1 cells surrounded by sustentacular or type 2 cells. This study aimed to analyze the morphological and functional changes that occur in CC, caused by hypertension induced by L-NAME, an inhibitor of nitric oxide synthase. For that, the study used 20 rats divided into two groups: control (C) and L-NAME (LN). After administration of 40mg/kg/day L-NAME for 45 days, the CC was collected. We observed significantly increased blood pressure starting at second week of administration of L-NAME. Quantitative analysis showed a reduction in the number of cells in the carotid glomus and an increase in the total area of the body in the LN group. No significant difference was found in the nuclei total number in carotid body between the groups. In the morphological analysis of the LN group, we observed the formation of vacuoles in type 1 glomus cells, as well as a reduction in the total number of nuclei of cells from each carotid glomus. The qualitative analysis suggested an increase in collagen and elastic system fibers in the extracellular matrix and cytoplasmic granules in LN group. Immunostainings with anti-VEGF and NFkappa- B and nNOS show was increase and dispersed in the LN group than in group C. In addition, appointments for P substance were also obeservado in greater amounts in type 1 cells of the LN group. The marking for PGP 9.5, there was a reduction of this marking characterized in carotid glomus LN group compared with group C. The study suggests that the carotid body, in response to hypertension induced by inhibition of nitric oxide synthase, produces morphophysiological changes similar to those found in hypoxia.