PMID- 16910158
OWN - NLM
STAT- MEDLINE
DCOM- 20061101
LR  - 20101118
IS  - 0870-2551 (Print)
IS  - 0870-2551 (Linking)
VI  - 25
IP  - 5
DP  - 2006 May
TI  - Morphologic, molecular and hemodynamic cardiac alterations in a model of 
      nephropathy induced by puromycin aminonucleoside.
PG  - 509-18
AB  - INTRODUCTION: Proteinuria and decreased glomerular filtration rate are assuming 
      increased importance in defining cardiovascular risk in chronic renal 
      insufficiency. The aim of this work was to study morphologic, molecular and 
      hemodynamic cardiac alterations in an animal model of proteinuria and renal 
      insufficiency induced by puromycin aminonucleoside (PAN). METHODS: Normotensive 
      rats (n = 14) were injected with PAN (150 mg/kg, i.p.) or with vehicle. Blood 
      pressure was measured daily and the animals were placed in metabolic cages for 
      evaluation of urinary excretion of sodium, protein and creatinine. Fourteen days 
      after PAN administration left ventricular hemodynamics were evaluated through a 
      pressure tip micromanometer and heart morphology was examined. Transmural samples 
      of left ventricle were then taken for mRNA quantification of SERCA2a, 
      phospholamban (PLB), insulin-like growth factor 1 (IGF-1) and 
      glyceraldehyde-3-phosphate dehydrogenase (GAPDH). RESULTS: The animals treated 
      with PAN presented a decrease in creatinine clearance (14th day: 2.24 +/- 0.32 
      vs. 4.51 +/- 1.08 ml/min) and an increase in proteinuria (14th day: 51.0 +/- 9.0 
      vs. 3.8 +/- 0.7 mg/mg creatinine), without changes in systolic (14th day: 151 +/- 
      7 vs. 141 +/- 6 mmHg) or diastolic blood pressure (14th day: 85 +/- 7 vs. 86 +/- 
      3 mmHg), These alterations were accompanied by cardiac atrophy with decreased 
      left ventricular contractility. A reduction in the SERCA2a/PLB mRNA ratio was 
      observed without significant alteration in the expression of IGF-1 in the left 
      ventricle. CONCLUSIONS: PAN-induced nephropathy is accompanied by cardiac 
      atrophy, left ventricular dysfunction and alterations in the expression of genes 
      involved in myocardial calcium kinetics. These findings were not accompanied by 
      increases in blood pressure and may contribute to our understanding of the 
      increased cardiovascular risk in chronic renal insufficiency.
FAU - Moreira-Rodrigues, M
AU  - Moreira-Rodrigues M
AD  - Unidade de Investigacao e Desenvolvimento de Nefrologia, Servico de Fisiologia, 
      Faculdade de Medicina, Universidade do Porto, Porto, Portugal.
FAU - Roncon-Albuquerque, R Jr
AU  - Roncon-Albuquerque R Jr
FAU - Henriques-Coelho, T
AU  - Henriques-Coelho T
FAU - Sampaio-Maia, B
AU  - Sampaio-Maia B
FAU - Leite-Moreira, A
AU  - Leite-Moreira A
FAU - Pestana, Manuel
AU  - Pestana M
LA  - eng
LA  - por
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Portugal
TA  - Rev Port Cardiol
JT  - Revista portuguesa de cardiologia : orgao oficial da Sociedade Portuguesa de 
      Cardiologia = Portuguese journal of cardiology : an official journal of the 
      Portuguese Society of Cardiology
JID - 8710716
RN  - 58-60-6 (Puromycin Aminonucleoside)
SB  - IM
MH  - Animals
MH  - Disease Models, Animal
MH  - Hemodynamics
MH  - *Proteinuria/chemically induced/metabolism/pathology/physiopathology
MH  - Puromycin Aminonucleoside/administration & dosage
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - *Renal Insufficiency/chemically induced/metabolism/pathology/physiopathology
EDAT- 2006/08/17 09:00
MHDA- 2006/11/02 09:00
CRDT- 2006/08/17 09:00
PHST- 2006/08/17 09:00 [pubmed]
PHST- 2006/11/02 09:00 [medline]
PHST- 2006/08/17 09:00 [entrez]
PST - ppublish
SO  - Rev Port Cardiol. 2006 May;25(5):509-18.