Protein remodeling of the heart ventricles in hereditary hypertriglyceridemic rat: effect of ACE-inhibition.
The aim of this study was to determine whether protein remodeling of the heart ventricles and remodeling of the aorta were present in hereditary hypertriglyceridemic (hHTG) rats and whether treatment with the angiotensin-converting enzyme inhibitor, captopril could prevent these alterations. Three groups of rats were investigated in a four week experiment control Wistar /C/rats, hHTg rats, hHTg rats given captopril (100 mg/kg/day) (hHTg + CAP). In the hHTg group, the increased systolic blood pressure (SBP) was associated with hypertrophy of the LV and RV. Protein profile analysis revealed an enhancement of metabolic protein concentration in both ventricles. The concentration of total collagenous proteins was not changed in either ventricles. However, alterations in composition of cardiac collagen were detected, characterized by higher concentration of hydroxyproline in pepsin-insoluble fraction and lower concentration of hydroxyproline in pepsin soluble faction in the LV. Hypertrophy of aorta, associated with the reduction of nitric oxide dependent relaxation, was also present in hHTG rats. Captopril normalized SBP, reduced left ventricular hypertrophy (LVH), diminished metabolic protein concentration in both ventricles, and improved NO-dependent relaxation of the aorta. Furthermore, captopril partially reversed alterations in hydroxyproline concentration in soluble and insoluble collagenous fractions of the LV. We conclude that hypertrophy of both ventricles and the aorta are present in hHTG rats, along with protein remodeling of both ventricles. Captopril partially prevented left ventricular hypertrophy development and protein remodeling of the myocardium.
Simko
Fedor
F
Department of Pathophysiology and 3rd Clinic of Medicine, Comenius University, School of Medicine, Bratislava, Slovak Republic. fedor.simko@fmed.uniba.sk
Pelouch
Václav
V
Torok
Jozef
J
Luptak
Ivan
I
Matuskova
Jana
J
Pechanova
Olga
O
Babal
Pavel
P
D000109:Acetylcholine / Q000494:pharmacology; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000378:metabolism*; D000818:Animals; D001011:Aorta / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D001794:Blood Pressure; D002216:Captopril / Q000378:metabolism*; D006352:Heart Ventricles / Q000737:chemistry* / Q000166:cytology / Q000378:metabolism*; D015228:Hypertriglyceridemia / Q000235:genetics / Q000378:metabolism*; D066298:In Vitro Techniques; D008297:Male; D009119:Muscle Contraction; D009126:Muscle Relaxation; D009929:Organ Size; D011506:Proteins / Q000032:analysis*; D051381:Rats; D017208:Rats, Wistar; D014665:Vasodilator Agents / Q000494:pharmacology; D020257:Ventricular Remodeling / Q000502:physiology*
D000806:Angiotensin-Converting Enzyme Inhibitors; D011506:Proteins; D014665:Vasodilator Agents; D002216:Captopril; D000109:Acetylcholine