Key result
Vitamin D deficiency in growing male rats increased systolic blood pressure and vascular oxidative stress, but slightly improved maximal relaxation to acetylcholine (83% vs 75%; P<0.05).
Why the study?
Does a vitamin D-deficient diet increase blood pressure, vascular oxidative stress, and alter cardiac gene expression in growing male rats?
Does a vitamin D-deficient diet increase blood pressure, vascular oxidative stress, and alter cardiac gene expression in growing male rats?
Absolute Event Rate: 83% vs 75%
p-value: p=<0.05
In a rat model, vitamin D deficiency increases arterial blood pressure and vascular oxidative stress while altering cardiac gene expression, though endothelial-mediated vasomotor tone is maintained via an NO-independent compensatory pathway.
Animal VDD data should not alter clinical practice; leaves open translation to human cardiovascular outcomes.
Vitamin D deficiency (VDD) is associated with an increased cardiovascular risk. We investigated the effect of VDD on the cardiovascular system of growing male rats fed with a vitamin D-deficient diet. Using isolated rat aorta, we assessed both superoxide anion and endothelial-dependent relaxations. Microarray technology was used to identify changes induced by VDD in cardiac gene expression. Compared with control, VDD increased systolic blood pressure (P < 0.05) and superoxide anion production in the aortic wall (P < 0.05) and tended to increase serum levels of angiotensin II and atrial natriuretic peptide (P < 0.15). However, VDD slightly improved maximal relaxation to acetylcholine from 75 % ± 3% to 83% ± 2% (P < 0.05). Incubation of aortic rings either with nitro-l-arginine methyl ester (l-NAME) or catalase did not eliminate the enhancement of endothelial-mediated relaxation observed in vitamin D-deficient rats. Only incubation with indometacin or calcium-activated potassium channels blockers suppressed this difference. Compared with control, the expression of 51 genes showed different expression, including several genes involved in the regulation of oxidative stress and myocardial hypertrophy. In conclusion, VDD in early life increases arterial blood pressure, promotes vascular oxidative stress, and induces changes in cardiac gene expression. However, the endothelial-mediated regulation of vasomotor tone is maintained throughout the enhancement of an NO-independent compensatory pathway.
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Argacha et al. (2011) studied Vitamin D deficiency. Vitamin D-deficient diet vs. Control was evaluated on Maximal relaxation to acetylcholine (p=<0.05). Vitamin D deficiency in growing male rats increased systolic blood pressure and vascular oxidative stress, but slightly improved maximal relaxation to acetylcholine (83% vs 75%; P<0.05).
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