Key result
L-NAME induces aortic remodelling driven by nitric oxide deficiency rather than hypertension.
Why the study?
It was unclear whether decreased nitric oxide synthase production or L-NAME-induced hypertension was responsible for metabolic and structural remodelling of the rat aorta during long-term L-NAME treatment.
Does L-NAME treatment induce structural remodelling of the rat aorta via NO deficiency or hypertension?
Does L-NAME treatment induce structural remodelling of the rat aorta via NO deficiency or hypertension?
Aortic remodelling in L-NAME-treated rats appears to be driven primarily by nitric oxide deficiency rather than the induced hypertension.
Answers are grounded in this paper and cite their sources.
Implicates nitric oxide deficiency over hypertension in L-NAME aortic remodeling; hypothesis-generating for human vascular mechanisms.
The aim of the present study was to determine whether decreased nitric oxide (NO) synthase production or rather NG-nitro-L-arginine methyl ester (L-NAME)-induced hypertension was responsible for metabolic and structural remodelling of the rat aorta during four-week L-NAME treatment. Three groups of male Wistar rats were investigated: control, treated with 20 mg/kg per day L-NAME (L-NAME20), and treated with 40 mg/kg per day L-NAME (L-NAME40). Systolic blood pressure significantly increased in L-NAME20 to 146% and in L-NAME40 to 149% of the control value. NO synthase activity in the aorta significantly decreased in L-NAME20 and L-NAME40 to 86% and 65% of the control values, respectively. Proteosynthesis was significantly elevated in both L-NAME groups, while nuclear DNA concentration was significantly elevated only in the L-NAME40 group. Cyclic GMP concentration significantly decreased in L-NAME20 to 73% and in L-NAME40 to 46% of the control. Cyclic AMP concentration significantly increased in L-NAME20 and L-NAME40 to 128% and 145% of the control value, respectively. The diameter and wall thickness-to-diameter ratio were significantly elevated only in the L-NAME40 group. We conclude that remodelling of the aorta in L-NAME-treated rats was rather associated with NO deficiency than L-NAME-induced hypertension.
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Bernátová et al. (1999) studied L-NAME-induced hypertension and aortic remodelling. L-NAME (NG-nitro-L-arginine methyl ester) vs. Control was evaluated on Structural and metabolic remodelling of the rat aorta. Four-week treatment with L-NAME in male Wistar rats induced aortic remodelling that was associated with nitric oxide deficiency rather than L-NAME-induced hypertension.
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