Effects of vitamin E deficiency on vasomotor activity and ultrastructural organisation of rat thoracic aorta

Abstract

1 The effects of vitamin E deficiency were evaluated in aortic rings isolated from rats maintained on a diet deficient in vitamin E. 2 Endothelium-dependent vasodilator responses to acetylcholine (ACh) and calcium ionophore, A23187, were reduced in preparations from treated animals, compared to the age-matched controls. The maximal vasodilatation to ACh was 66.4 ± 9 (n = 4) and 38.8 ± 7 (n = 4) % in control and 10 monthtreated preparations, respectively. 3 The endothelium-independent vasodilator responses to sodium nitroprusside as well as the concentration-dependent contractile responses to noradrenaline, did not differ between treated and control preparations. 4 Electron microscopic examination of vascular segments and revealed that, following vitamin E deficiency, normal tissue organisation was disrupted, the endothelial monolayer either not being in contact with the underlying tissue or being absent in most of the areas analysed. 5 It is concluded that during vitamin E deficiency both morphological disruption and functional impairment of endothelium occur without observable modification of muscle cell function and morphology.

Effect of Chronic Treatment with Vitamin E on Endothelial Dysfunction in a Type I in Vivo Diabetes Mellitus Model and in Vitro

“…Interestingly, although this was not affected by high vitamin E treatment, vitamin E deficiency further diminished vasorelaxant response to GTN and completely abolished relaxation to ACh, with a reversal of the ACh-response so that vasoconstriction occurred. It should be mentioned that vitamin E deprivation for 4 to 12 months itself impairs endothelial relaxation, whereas smooth muscle responses are not affected (Rubino and Burnstock, 1994;Rubino et al, 1995;Ralevic et al, 1995). These investigators, however, observed only reduced vasorelaxation in vitamin E deprivation.…”