LEANDRO EZIQUIEL DE SOUZA
Índice h a partir de 2011
7
Projetos de Pesquisa
Unidades Organizacionais
Instituto do Coração, Hospital das Clínicas, Faculdade de Medicina
4 resultados
Resultados de Busca
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- Acute renal denervation normalizes aortic function and decreases blood pressure in spontaneously hypertensive rats(2020) MOREIRA, Nathalia Juocys Dias; SANTOS, Fernando dos; MOREIRA, Edson Dias; FARAH, Daniela; SOUZA, Leandro Eziquiel de; SILVA, Maikon Barbosa da; MORAES-SILVA, Ivana Cinthya; LINCEVICIUS, Gisele Silverio; CALDINI, Elia Garcia; IRIGOYEN, Maria Claudia CostaMechanisms involved in the acute responses to renal denervation (RDN) have yet to be fully understood. We assessed urinary volume, autonomic control and aorta vascular reactivity after acute RDN. Male normotensive Wistar rats and spontaneously hypertensive rats (SHR) were divided into normotensive+RDN (ND) or sham surgery (NS), and hypertensive+RDN (HD) or sham surgery (HS). Metabolic parameters and hemodynamic measurements were recorded 72h and 4 days after intervention, respectively. Aortic rings were studied 7 days post RDN in an isometric myograph. Concentration-response curves to phenylephrine, sodium nitroprusside and acetylcholine (10(-10)-10(-5) M) were performed. Two-way ANOVA was used for group comparisons and differences reported when p < 0.05. Results are presented as mean +/- SEM. Urinary volume was 112% higher in HD vs. HS (HS=14.94 +/- 2.5 mL; HD=31.69 +/- 2.2 mL) and remained unchanged in normotensive rats. Systolic BP was lower in HD rats (HS=201 +/- 12 vs. HD=172 +/- 3 mmHg) without changes in normotensive group. HD group showed increased HF and LF modulation (HS=5.8 +/- 0.7 ms(2) vs. HD=13.4 +/- 1.4 ms(2); HS=3.5 +/- 0.7 ms(2) vs. HD=10.5 +/- 1.7 ms(2), respectively). RDN normalized vascular reactivity in HD rats and increased phenylephrine response in ND rats. Acute fall in BP induced by RDN is associated with increased urinary volume, which in turn may also have contributed to functional changes of the aorta.
conferenceObject CARDIORENAL DYSFUNCTION IN MICE SUBMITTED TO AORTIC STENOSIS AND TREATED WITH SODIUM OXALATE(2023) SILVA, Amanda; MARQUES, Juliana; NASCIMENTO, Bruno; SOUZA, Leandro; SILVA, Maikon; BENETTI, Acaris; IRIGOYEN, Maria ClaudiaconferenceObject Acute vascular and autonomic responses of renal denervation in spontaneously hypertensive rats(2017) MOREIRA, N. J. D.; SANTOS, F. Dos; MOREIRA, E. D.; FARAH, D.; SOUZA, L. E. De; SILVA, M. B. Da; IRIGOYEN, M. C.- Proinflammatory Role of Angiotensin II in the Aorta of Normotensive Mice(2019) LIMA, Rariane Silva de; SILVA, Juliane Cristina de Souza; LIMA, Cintia Taniguti; SOUZA, Leandro Ezequiel de; SILVA, Maikon Barbosa da; BALADI, Marina Gazzano; IRIGOYEN, Maria Claudia; LACCHINI, SilviaAngiotensin II plays important functions in cardiovascular system mediating actions leading to inflammatory responses such as activation of VSMC in order to produce ROS, inflammatory cytokines, chemokines, and adhesion molecules. Changes in angiotensin II production could stimulate the recruitment and activation of myeloid cells initiating local inflammatory response without effect on BP. We aimed to verify if angiotensin II induces an inflammatory response in the aorta and if it correlates with variations in BP. C57Bl/6 mice treated with saline solution (0.9%, control group) or angiotensin II (30ng/kg, Ang II group) were used. BP and HR levels were measured. Immunohistochemistry for IL1-, TGF-, iNOS, CD45, and -actin was performed in the aorta. BP and HR do not change. A biphasic response was observed both for IL1- and TGF- expression and also for the presence of CD45 positive cells, with an acute increase (between 30 and 60 minutes) and a second increase, between 24 and 48 hours. Positive staining for iNOS increased in the earlier period (30 minutes) in perivascular adipose tissue and in a longer period (48 hours) in tunica adventitia. Immunoblotting to -actin showed no alterations, suggesting that the applied dose of angiotensin II does not alter the aortic VSMCs phenotype. The results suggest that angiotensin II, even at doses that do not alter BP, induces the expression of inflammatory markers and migration of inflammatory cells into the aorta of normotensive mice. Thus, angiotensin II may increase the propensity to develop a cardiovascular injury, even in normotensive individuals.