: Beneficial cardiac effects of enalapril in postmenoapusal hypertensive rats

ZILBERMAN J; YAÑES L; TOMAT AL; ROMERO M; SARTORI-VALLINOTTI; ELESGARAY R; COSTA M.A; RECKELFOFF J; ARRANZ C

New Orleans, Lousiana, USA

Congreso; Experimental Biology; 2009

FASEB (Federation of American Societies for Experimental Biology) Office of Scientific Meetings and Conferences

SEVERAL STUDIES SUGGEST AN INTERACTION BETWEEN RENIN-ANGIOTENSIN SYSTEM AND ESTRAGEN WITH NITRIC OXIDE (NO) SYSTEM AND OXIDATIVE STRESS. OBJECTIVE: TO EVALUATE THE EFFECTS OF THE  ANGIOTENSIN-CONVERTING ENZYME INHIBITOR ENALAPRIL (E) ON SYSTOLIC BLOOD PRESSURE (SBP), OXIDATIVE STRESS, NO SYNTHASE (NOS) ACTIVITY AND ESTROGEN RECEPTOR EXPRESSION IN THE LEFT VENTRICLE  OF POSTMENOPAUSAL SPONTANEOUSLY HYPERTENSIVE RATS (OF-SHR). AGED 16 MONTHS RECIEVED E250 MG/L IN DRINKING WATER OR TAP WATER (C) FOR 30 DAYS. AT THE END OF THE TREATMENT LIPID PEROXIDATION END PRODUCTS (TBARS), ESTROGEN RECEPTOR EXPRESSION, CATALASE (CAT), GLUTATHION PEROXIDASE (GPX) AND NOS ACTIVITY WERE MEASURED IN LV. RESULTS: TREATMENT WITH ENALAPRIL DECREASED SBP AND TBARS BUT INCREASED GPX AND NOS ACTIVITY IN OF-SHR. ESTROGEN  RECEPTOR B WAS UPREGULATED BY E TREATMENT IN LV OF OF-SHR   SBP (mmHg) TBARS (ng/mg.prot) CAT (pmol/mg.prot) GPx (pmol/min.mg. prot) NOS activity (pmol.citrulline 14C/g tissue. min) C 174±8 0.215±0.029 0.062±0.006 2.30±0.10 348.1±3.8 E 152±9# 0.137±0.006* 0.039±0.009* 2.94±0.20* 445.3±13.5* * P<0.02 OR #P<0.01 VS CONTROL. IN CONCLUSION OUR STUDY SHOWS THAT ENALAPRIL ADMINISTRATION CAUSED A REDUCTION IN OXIDATIVE STRESS AND INCREASES IN NOS ACTIVITY AND ESTROGEN RECEPTOR B EXPRESSION IN LV OF OF-SHR. THESE RESULTS SUGGEST THAT CHANGES OBSERVED IN LV AFTER MENOPAUSE MAY ANGIOTENSINE II MEDIATED.