Effect of chronic vitamin E deficiency on sympathetic and sensorimotor function in rat mesenteric arteries.

1. Mesenteric arterial beds from male rats deprived of vitamin E for 12 months postweaning were isolated and perfused at 5 ml min‐1. 2. The basal perfusion pressure of vitamin E‐deficient preparations was significantly higher (34.0 +/‐ 1.9 mmHg, n = 15) than in age‐matched controls (26.1 +/‐ 2 mmHg, n = 14; P < 0.01). 3. At basal tone, vasoconstrictor responses to electrical field stimulation (EFS) were not attenuated by vitamin E deficiency; at high stimulation frequencies, responses were enhanced. According to dose‐response curves, exogenous noradrenaline was significantly more efficacious in preparations from vitamin E‐deficient rats (P < 0.05). 4. In preparations with tone raised by methoxamine (6‐20 microM) and in the presence of guanethidine (5 microM), EFS of perivascular sensorimotor nerves elicited frequency‐dependent vasodilatation which was significantly attenuated by vitamin E deficiency. There was no difference in relaxation to calcitonin gene‐related peptide (CGRP; 1.5 x 10(‐11) mol), or to the sensory neurotoxin capsaicin (5 x 10(‐11) mol). 5. Immunohistochemical analysis of CGRP‐containing nerves in the superior mesenteric artery showed no differences in density of innervation. 6. In conclusion, chronic vitamin E deficiency impairs sensorimotor vasodilatation in rat mesenteric arteries; this does not appear to be due to changes in postjunctional receptors, or to a depletion of transmitter (CGRP) content of the superior mesenteric artery. Sensorimotor nerves appear to be more vulnerable than sympathetic nerves to chronic vitamin E deficiency.