RGD Reference Report - Lisinopril reduces cardiac hypertrophy and mortality in rats with aortocaval fistula. - Rat Genome Database

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Lisinopril reduces cardiac hypertrophy and mortality in rats with aortocaval fistula.

Authors: Oka, T  Nishimura, H  Ueyama, M  Kubota, J  Kawamura, K 
Citation: Oka T, etal., Eur J Pharmacol. 1993 Mar 30;234(1):55-60.
RGD ID: 12880017
Pubmed: PMID:8386093   (View Abstract at PubMed)

We evaluated the effects of lisinopril (1 mg/kg per day) on hemodynamics, cardiac hypertrophy, and neurohumoral factors in Wistar rats with an abdominal aortocaval fistula. After 4 weeks of treatment, the results were compared with values obtained for untreated rats with a fistula and for sham-operated rats. Volume loading induced biventricular hypertrophy, hemodynamic signs of high-output heart failure (increased cardiac output, left ventricular end-diastolic pressure, and pulse pressure), and impaired renal function (decreased renal blood flow and kidney weight; increased blood urea nitrogen). Lisinopril did not affect these cardiorenal hemodynamics, but decreased left ventricular mass and mortality rate (both P < 0.05). Lisinopril attenuated the increase in plasma norepinephrine, and increased plasma renin activity (both P < 0.05). Thus, lisinopril reduced left ventricular mass and mortality in rats with high-output heart failure without changing the cardiorenal hemodynamics. Neurohumoral inhibition may play a role in the beneficial effects of lisinopril.




  
Object Symbol
Species
Term
Qualifier
Evidence
With
Notes
Source
Original Reference(s)
ACEHumanArteriovenous Fistula treatmentISOAce (Rattus norvegicus) RGD 
AceRatArteriovenous Fistula treatmentIMP  RGD 
AceMouseArteriovenous Fistula treatmentISOAce (Rattus norvegicus) RGD 


Genes (Rattus norvegicus)
Ace  (angiotensin I converting enzyme)

Genes (Mus musculus)
Ace  (angiotensin I converting enzyme)

Genes (Homo sapiens)
ACE  (angiotensin I converting enzyme)