Key result
Spironolactone normalized left ventricular mass in L-NAME-induced hypertensive rats but failed to reverse contractile, metabolic, and collagenous protein remodeling, unlike spontaneous or L-arginine-induced regression.
Why the study?
Does spironolactone or L-arginine reverse left ventricular protein remodeling in rats with L-NAME-induced hypertension?
Does spironolactone or L-arginine reverse left ventricular protein remodeling in rats with L-NAME-induced hypertension?
In a rat model of L-NAME-induced hypertension, spironolactone effectively reduces left ventricular hypertrophy but may not fully normalize myocardial protein concentrations, possibly due to reduced myocardial water content.
Answers are grounded in this paper and cite their sources.
Spironolactone may normalize LV mass without reversing protein remodeling in this model; leaves open whether L-arginine yields more complete regression.
N(G)-nitro-L-arginine-methyl ester (L-NAME)-induced hypertension is associated with protein remodeling of the left ventricle. The aim of the study was to show, whether aldosterone receptor blocker spironolactone and precursor of NO-production L-arginine were able to reverse the protein rebuilding of the left ventricle. Six groups of male Wistar rats were investigated: control 4 (4 weeks placebo), L-NAME (4 weeks L-NAME), spontaneous-regression (4 weeks L-NAME + 3 weeks placebo), spironolactone-regression (4 weeks L-NAME + 3 weeks spironolactone), L-arginine-regression (4 weeks L-NAME + 3 weeks arginine), control 7 (7 weeks placebo). L-NAME administration induced hypertension, hypertrophy of the left ventricle (LV), and the increase of metabolic and contractile as well as soluble and insoluble collagenous protein concentration. The systolic blood pressure and relative weight of the LV decreased in all three groups with regression, while the most prominent attenuation of the LVH was observed after spironolactone treatment. In the spontaneous-regression and L-arginine-regression groups the concentrations of individual proteins were not significantly different from the control value. However, in the spironolactone-regression group the concentration of metabolic, contractile and insoluble collagenous proteins remained significantly increased in comparison with the control group. The persistence of the increased protein concentration in the spironolactone group may be related to the more prominent reduction of myocardial water content by spironolactone.
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Šimko et al. (2007) studied L-NAME-induced hypertension and left ventricular hypertrophy (n=52). Spironolactone and L-arginine vs. Placebo was evaluated on Left ventricular relative weight and protein concentration. Spironolactone normalized left ventricular mass in L-NAME-induced hypertensive rats but failed to reverse contractile, metabolic, and collagenous protein remodeling, unlike spontaneous or L-arginine-induced regression.
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