RGD Reference Report - Lisinopril reduces cardiac hypertrophy and mortality in rats with aortocaval fistula. - Rat Genome Database
Submit Data |  Help |  Video Tutorials |  News |  Publications |  Download |  REST API |  Citing RGD |  Contact   

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: (View Article at PubMed) PMID:8386093

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.


Disease Annotations    

Objects Annotated

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

Genes (Mus musculus)
Ace  (angiotensin I converting enzyme (peptidyl-dipeptidase A) 1)

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

Additional Information