Cardiac and pulmonary arterial remodeling after sinoaortic denervation in normotensive rats

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art_FLUES_Cardiac_and_pulmonary_arterial_remodeling_after_sinoaortic_denervation_2012.PDF (936.58 KB)
Citações na Scopus
16
Tipo de produção
article
Data de publicação
2012
DOI
Scopus
Web of Science
PubMed
Título da Revista
ISSN da Revista
Título do Volume
Editora
ELSEVIER SCIENCE BV
Autores
DINIZ, G. P.
PIRATELLO, A. C.
CHAVES, M. L. Barreto
Citação
AUTONOMIC NEUROSCIENCE-BASIC & CLINICAL, v.166, n.1-2, p.47-53, 2012
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
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.
Palavras-chave
Baroreflex, Autonomic nervous system, Hypertension, Cardiac remodeling, Pulmonary artery remodeling, Pulmonary hypertension
URI
https://observatorio.fm.usp.br/handle/OPI/990
Referências
  1. Agabiti-Rosei E., 2007, THER ADV CARDIOVASC, V2, P119
  2. Bertagnolli M., 2008, AM J HYPERTENS, V11, P1188
  3. Brum PC, 2000, HYPERTENSION, V36, P1018
  4. Franchini K.G., 1994, AM PHYSL SOC, p[0363, 94]
  5. Gerritsen J, 2001, DIABETES CARE, V24, P1793, DOI 10.2337/diacare.24.10.1793
  6. Grassi G, 2009, HYPERTENSION, V53, P205, DOI 10.1161/HYPERTENSIONAHA.108.121467
  7. Hardziyenka M, 2006, J AM SOC ECHOCARDIOG, V19, P1272, DOI 10.1016/j.echo.2006.04.036
  8. Heeren MV, 2009, MATURITAS, V62, P200, DOI 10.1016/j.maturitas.2008.12.011
  9. Hisashi K., 2009, CIRC J, V73, P2198
  10. Irigoyen MC, 2005, HYPERTENSION, V46, P998, DOI 10.1161/01.HYP.0000176238.90688.6b
  11. IRIGOYEN MC, 1995, HYPERTENSION, V26, P1111
  12. JUDY WV, 1979, HYPERTENSION, V1, P605
  13. Junqueira L.C., 1979, HISTOCHEM J, V4, P447
  14. Koskenvuo JW, 2010, INT J CARDIOVAS IMAG, V26, P509, DOI 10.1007/s10554-010-9596-1
  15. KRIEGER EM, 1964, CIRC RES, V15, P511
  16. KRIEGER EM, 1963, AM J PHYSIOL, V205, P771
  17. Kudo H, 2009, HYPERTENSION, V54, P832, DOI 10.1161/HYPERTENSIONAHA.109.135905
  18. Lang K.R., 2005, J AM SOC ECHOCARDIOG, P18
  19. La Rovere MT, 1998, LANCET, V351, P478
  20. Liu AJ, 2007, STROKE, V38, P1916, DOI 10.1161/STROKEAHA.106.480061
  21. Miao C.V., 2006, HYPERTENSION, V6, P1125
  22. Miao CY, 2002, J HYPERTENS, V20, P1865, DOI 10.1097/00004872-200209000-00033
  23. Miao CY, 2003, AM J HYPERTENS, V16, P585, DOI 10.1016/S0895-7061(03)00866-5
  24. Miao CY, 2004, CLIN EXP PHARMACOL P, V31, P450, DOI 10.1111/j.1440-1681.2004.04023.x
  25. Malliani Alberto, 2002, Ital Heart J, V3, P439
  26. O'Leary D.M., 2004, RESP PHYSIOL NEUROBI, P137
  27. Piratello AC, 2010, CLINICS, V65, P1345, DOI 10.1590/S1807-59322010001200019
  28. SASAKI S, 1994, AM J HYPERTENS, V7, P453
  29. Schwartz PJ, 1998, EUR HEART J, V19, P1593, DOI 10.1053/euhj.1998.1292
  30. Souza S.B., 2007, HYPERTENSION, V4, P786
  31. Su DF, 2001, CLIN EXP PHARMACOL P, V28, P709, DOI 10.1046/j.1440-1681.2001.03508.x
  32. Tao Xia, 2008, J Cardiovasc Pharmacol, V51, P24, DOI 10.1097/FJC.0b013e318159e097
  33. Thibault HB, 2010, CIRC-CARDIOVASC IMAG, V3, P157, DOI 10.1161/CIRCIMAGING.109.887109
  34. Van Vliet BN, 1999, J PHYSIOL-LONDON, V516, P885
  35. Vikstrom KL, 1998, CIRC RES, V82, P773
  36. Wichi R, 2007, CARDIOVASC DIABETOL, V6, DOI 10.1186/1475-2840-6-14
  37. Xie LD, 2010, CLIN EXP HYPERTENS, V32, P547, DOI 10.3109/10641963.2010.503295

Coleções
Artigos e Materiais de Revistas Científicas - FM/MPT
Artigos e Materiais de Revistas Científicas - FM/MCP
Artigos e Materiais de Revistas Científicas - HC/InCor
Artigos e Materiais de Revistas Científicas - LIM/11
Artigos e Materiais de Revistas Científicas - LIM/59