Abstract P055: Systemic Arterial Hypertension Induces Pulmonary Injury Beyond Protein Degradation and Atrophy of Diaphragm
Background: Systemic arterial hypertension (SAH) is a chronic disease associated with systemic inflammation. Although cardiovascular adaptations resulting from SAH are more evident, little is known about the respiratory alterations. The purinergic receptor P2X7 plays a key role in the immune modulation, beyond to control the vascular tone and the development of inflammation and fibrosis.
Aims: Evaluate the effects of SAH on the pulmonary inflammation and remodeling and on the diaphragm, and the involvement of purinergic receptor P2X7 and of ubiquitin-proteasome system (UPS) in this response.
Methods: Spontaneously hypertensive rats (SHR) and normotensive Wistar (N) with 18 weeks-of-age were evaluated for: inflammation and remodeling of airways and pulmonary vessels and for P2X7 receptor expression. The morphology and biochemistryin diaphragm muscle for myosin ATPase reaction and ubiquitin-proteasome system (UPS), respectively.
Results: The SHR showed a higher wall/lumen of the pulmonary arteries, as well as increased collagen deposition on the wall of these arteries. Increase in P2X7 receptor expression in pulmonary vascular wall (SHR:4.3%±0.7% vs. N:0.3%±0.2%) and bronchial epithelial (SHR:29±0% vs 2.8% N:10.5%±1.3%). The diaphragm was increased cross-sectional area (CSA) of type I fibers (16%) and reduction in CSA of type II (41%), increased the UPS activity and lipid peroxidation. SHR did not change in the analysis of ubiquitinated proteins and misfolded proteins.
Conclusion: SAH induces important pulmonary disorders such pulmonary vascular remodeling, with increased expression of the purinergic receptor P2X7 associated with atrophy and protein degradation on diaphragm.
Author Disclosures: P.R.M. Souza: None. R.P. Vieira: None. K. Flues: None. W.M.A.M. De-Moraes: None. J.B. Ferreira: None. A. Medeiros: None. K. De Angelis: None. F.M. Consolim-Colombo: None. M.C. Irigoyen: None.
- © 2015 by American Heart Association, Inc.