1. Male rats were deprived as weanlings of dietary
vitamin E for 2, 4, 6, 10 and 12 months. Mesenteric arterial beds from these rats and from age-matched controls were isolated and perfused with
Krebs solution at a constant flow rate (5 ml min-1). The function of perivascular sympathetic nerves, smooth muscle and endothelium was assessed. 2. At 12 months
vitamin E deficient rats exhibited the characteristic symptoms of
vitamin E deficiency, namely poor coat condition, muscle wasting, kyphoscoliosis and impaired gait. In the isolated mesenteric arterial bed electrical field stimulation (EFS) of perivascular nerves (4-32 Hz, 90 V, 1 ms, for 30 s) elicited frequency-dependent
vasoconstrictor responses which were unaffected by
vitamin E deficiency except at 12 months, at which age responses were significantly greater than those of the controls at 24 and 32 Hz (P < 0.01). 3. Exogenous
noradrenaline (NA; 0.15-500 nmol) elicited dose-dependent vasoconstriction which was similar in
vitamin E-deficient and control preparations at all ages.
Potassium chloride (0.15 mmol) also produced similar
vasoconstrictor responses in
vitamin E-deficient and control preparations at each age. 4. Tone of the preparations was raised by continuous perfusion with
methoxamine (4-70 microM), producing similar increases in perfusion pressure in
vitamin E-deficient and control preparations at each age. Endothelium-dependent dose-dependent vasodilatation to
adenosine 5'-triphosphate was significantly impaired in mesenteric arterial beds from 12 month-old
vitamin E-deficient rats compared with the controls (P < 0.05). Relaxation to
acetylcholine was not significantly different at any age. 5. Endothelium-independent vasodilatation to
sodium nitroprusside was similar in
vitamin E-deficient rats and age-matched controls. 6. These results suggest that long term (12 months) deprivation of dietary
vitamin E may impair endothelial function in mesenteric arteries of the rat. Sympathetic perivascular nerve constrictor function was increased at 12 months. There were no functionally expressed changes in the vascular smooth muscle, which appears to be more resilient to the effects of oxidative stress in
vitamin E deficiency.