Regression of chronic L -NAME-treatment-induced left ventricular hypertrophy: effect of captopril.
Long-term administration of N(G)-nitro- L -arginine methyl ester (L -NAME) induces development of NO-deficient hypertension and left ventricular (LV) hypertrophy. In this work, we examined the effect of spontaneous and captopril-induced recovery on LV hypertrophy and protein composition in rats with developed L -NAME-induced hypertension. Four groups of rats were investigated: control L -NAME 40 mg/kg/day for 4 weeks (L -NAME) L -NAME 40 mg/kg/day for 4 weeks followed by 3-week spontaneous recovery (L -NAME+R) L -NAME 40 mg/kg/day for 4 weeks followed by 3 weeks of captopril treatment at a dose of 100 mg/kg/day (L -NAME+C). LV hypertrophy in the L -NAME group was associated with an increase in content and concentration of left ventricular DNA and RNA, concentration of metabolic proteins (MP) and soluble collagenous proteins (SCP). Spontaneous recovery period reduced the hypertension, without regression of LV hypertrophy. Left ventricular DNA and RNA content were increased in the L -NAME+R group. In this group, concentrations of MP, contractile proteins (CP), and collagenous proteins did not differ from those in the L -NAME group. Captopril treatment caused total regression of hypertension and LV hypertrophy and decreased both content and concentration of DNA and RNA, as well as the contents of MP, CP and SCP v the L -NAME group. However, after captopril treatment, concentration of collagenous and non-collagenous protein fractions remained increased v control. We conclude that spontaneous regression of L -NAME-induced hypertension is not associated with regression of LV hypertrophy. LV hypertrophy was regressed only in captopril-treated animals.
Bernátová
I
I
Institute of Normal and Pathological Physiology, Comenius University, Bratislava, Slovak Republic. Bernat@unpf.savba.sk
Pechánová
O
O
Pelouch
V
V
Simko
F
F
D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*; D000818:Animals; D001835:Body Weight; D002216:Captopril / Q000494:pharmacology / Q000627:therapeutic use*; D003094:Collagen / Q000032:analysis; D004247:DNA / Q000032:analysis; D006352:Heart Ventricles / Q000737:chemistry / Q000187:drug effects / Q000473:pathology; D006973:Hypertension / Q000139:chemically induced; D017379:Hypertrophy, Left Ventricular / Q000139:chemically induced / Q000188:drug therapy* / Q000473:pathology; D008297:Male; D009124:Muscle Proteins / Q000032:analysis; D019331:NG-Nitroarginine Methyl Ester / Q000633:toxicity*; D009569:Nitric Oxide / Q000172:deficiency; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D009929:Organ Size; D012313:RNA / Q000032:analysis; D051381:Rats; D017208:Rats, Wistar; D012075:Remission, Spontaneous; D012084:Renin-Angiotensin System / Q000502:physiology; D020257:Ventricular Remodeling / Q000187:drug effects*
D000806:Angiotensin-Converting Enzyme Inhibitors; D009124:Muscle Proteins; D009569:Nitric Oxide; D012313:RNA; D003094:Collagen; D004247:DNA; D002216:Captopril; D019001:Nitric Oxide Synthase; D019331:NG-Nitroarginine Methyl Ester