Key result
In hereditary hypertriglyceridemic rats, captopril normalized systolic blood pressure and decreased left ventricular hypertrophy (LV/BW 1.44 vs 1.63 g/kg in untreated hHTg rats).
Why the study?
Does captopril and/or L-NAME affect left ventricular remodeling and blood pressure in hereditary hypertriglyceridemic rats?
Does captopril and/or L-NAME affect left ventricular remodeling and blood pressure in hereditary hypertriglyceridemic rats?
In a rat model of hereditary hypertriglyceridemia, ACE inhibition with captopril prevents left ventricular hypertrophy and fibrosis, suggesting a role for NO impairment and sympathoadrenal activation in this remodeling.
Supports ACE inhibition for LV remodeling in this rat model; leaves open translation to human hypertriglyceridemic hypertension.
AIM: The hereditary hypertriglyceridemic (hHTg) rat is characterized by insulin resistance, hypertension, and hypertriglyceridemia. Thus, we investigated whether (a) remodeling of the heart left ventricle (LV) is present under the given hypertensive situation and (b) whether this potential alteration could be influenced by an inhibition of the angiotensin converting enzyme (ACE) and/or by a blockade of nitric oxide production. METHODS: Five groups of rats were investigated: control Wistar (C) rats, hHTg rats, hHTg rats given captopril (100 mg/kg/day) (hHTg + CAP) or NG-nitro-l-arginine methyl ester (L-NAME, 40 mg/kg/day) (hHTg + L-NAME), and hHTg rats given the combination of both drugs (hHTg + CAP + L-NAME) for 28 days. Systolic blood pressure (SBP) was measured by tail-cuff plethysmography each week. After cervical dislocation, the relative weights of the left and right ventricles (LV/BW, RV/BW) were obtained, the LV nucleic acid concentrations were analyzed, and the fibrosis amount was quantified with aid of a semiquantitative histological technique. RESULTS: In the hHTg group, the increased SBP (141.7 +/- 4.4 vs. 117.2 +/- 3.1 mmHg in controls) was linked to hypertrophy of the LV (1.63 +/- 0.05 vs. 1.30 +/- 0.03 g/kg in controls) with only a minimum of fibrosis. DNA concentration in the LV was decreased (0.45 +/- 0.03 vs. 0.69 +/- 0.04 mg/g w.w. in controls) in the hHTg group. Captopril normalized SBP and decreased the LV/BW (1.44 +/- 0.04 g/kg). Chronic administration of L-NAME to the hHTg rats additionally enhanced (189.3 +/- 5.9 mmHg) the already raised SBP, stimulated fibrosis development, and increased DNA concentration (0.54 +/- 0.02 mg/g w.w.) in the LV compared to hHTg group, yet without additional weight increase of the LV. The combined treatment of the hHTg rats with CAP and L-NAME resulted in normal SBP and the development of LV hypertrophy, and fibrosis was substantially reduced. CONCLUSIONS: (a) The heart of hHTg rats carries signs of LV hypertrophy with minimal fibrosis. (b) Nevertheless, LV fibrosis was increased in the hHTg + L-NAME group. (c) Captopril normalized SBP and decreased the extent of LV hypertrophy in both the nontreated hHTg and the hHTg + L-NAME groups and (d) substantially reduced the development of LV fibrosis in the hHTg + L-NAME group. LVH in hHTg rats may be induced by sympathoadrenal system activation, circulating volume enlargement, and impairment of nitric oxide (NO) production rather than by activation of the renin-angiotensin-aldosterone system.
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Šimko et al. (2002) studied Hereditary hypertriglyceridemia and hypertension. Captopril and/or L-NAME vs. Control Wistar rats and untreated hHTg rats was evaluated on Systolic blood pressure and left ventricular hypertrophy (LV/BW). In hereditary hypertriglyceridemic rats, captopril normalized systolic blood pressure and decreased left ventricular hypertrophy (LV/BW 1.44 vs 1.63 g/kg in untreated hHTg rats).
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