Cardiac and pulmonary arterial remodeling after sinoaortic denervation in normotensive rats


Autoria(s): Flues, K.; Moraes-Silva, I. C.; Mostarda, C.; Souza, P. R. M.; Diniz, G. P.; Moreira, E. D.; Piratello, A. C.; Barreto Chaves, M. L.; De Angelis, K.; Cury Salemi, Vera Maria; Irigoyen, M. C.; Caldini, E. G.
Contribuinte(s)

UNIVERSIDADE DE SÃO PAULO

Data(s)

05/11/2013

05/11/2013

2012

Resumo

Blood pressure variability (BPV) and baroreflex dysfunction may contribute to end-organ damage process. We investigated the effects of baroreceptor deficit (10 weeks after sinoaortic denervation - SAD) on hemodynamic alterations, cardiac and pulmonary remodeling. Cardiac function and morphology of male Wistar intact rats (C) and SAD rats (SAD) (n = 8/group) were assessed by echocardiography and collagen quantification. BP was directly recorded. Ventricular hypertrophy was quantified by the ratio of left ventricular weight (LVW) and right ventricular weight (RVW) to body weight (BW). BPV was quantified in the time and frequency domains. The atrial natriuretic peptide (ANP), alpha-skeletal actin (alpha-skelectal), collagen type I and type III genes mRNA expression were evaluated by RT-PCR. SAD did not change BP, but increased BPV (11 +/- 0.49 vs. 5 +/- 0.3 mm Hg). As expected, baroreflex was reduced in SAD. Pulmonary artery acceleration time was reduced in SAD. In addition, SAD impaired diastolic function in both LV (6.8 +/- 0.26 vs. 5.02 +/- 0.21 mm Hg) and RV (5.1 +/- 0.21 vs. 4.2 +/- 0.12 mm Hg). SAD increased LVW/BW in 9% and RVW/BW in 20%, and augmented total collagen (3.8-fold in LV, 2.7-fold in RV, and 3.35-fold in pulmonary artery). Also, SAD increased type I (similar to 6-fold) and III (similar to 5-fold) collagen gene expression. Denervation increased ANP expression in LV (75%), in RV (74%) and increased a-skelectal expression in LV (300%) and in RV (546%). Baroreflex function impairment by SAD, despite not changing BP, induced important adjustments in cardiac structure and pulmonary hypertension. These changes may indicate that isolated baroreflex dysfunction can modulate target tissue damage. (C) 2011 Elsevier B.V. All rights reserved.

Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP)

Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP)

Fundacao Zerbini-Sao Paulo

Fundacao ZerbiniSao Paulo

Identificador

AUTONOMIC NEUROSCIENCE-BASIC & CLINICAL, AMSTERDAM, v. 166, n. 41306, supl. 1, Part 3, pp. 47-53, 46023, 2012

1566-0702

http://www.producao.usp.br/handle/BDPI/41931

10.1016/j.autneu.2011.10.005

http://dx.doi.org/10.1016/j.autneu.2011.10.005

Idioma(s)

eng

Publicador

ELSEVIER SCIENCE BV

AMSTERDAM

Relação

AUTONOMIC NEUROSCIENCE-BASIC & CLINICAL

Direitos

closedAccess

Copyright ELSEVIER SCIENCE BV

Palavras-Chave #BAROREFLEX #AUTONOMIC NERVOUS SYSTEM #HYPERTENSION #CARDIAC REMODELING #PULMONARY ARTERY REMODELING #PULMONARY HYPERTENSION #BLOOD-PRESSURE VARIABILITY #BAROREFLEX SENSITIVITY #CARDIOVASCULAR CONTROL #HYPERTENSIVE-RATS #HYPERTROPHY #DYSFUNCTION #MORTALITY #MARKERS #NEUROSCIENCES
Tipo

article

original article

publishedVersion