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 1 2 months postweaning were isolated and perfused at 5 ml min(-1). 2. Th e basal perfusion pressure of vitamin E-deficient preparations was sig nificantly higher (34.0 +/- 1.9 mmHg, n = 15) than in age-matched cont rols (26.1 +/- 2 mmHg, n = 14; P < 0.01). 3. At basal tone, vasoconstr ictor responses to electrical field stimulation (EFS) were not attenua ted by vitamin E deficiency; at high stimulation frequencies, response s were enhanced. According to dose-response curves, exogenous noradren aline was significantly more efficacious in preparations from vitamin E-deficient rats (P < 0.05). 4. In preparations with tone raised by me thoxamine (6-20 mu M) and in the presence of guanethidine (5 mu M), EF S of perivascular sensorimotor nerves elicited frequency-dependent vas odilatation which was significantly attenuated by vitamin E deficiency There was no difference in relaxation to calcitonin gene-related pept ide (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 dens ity of innervation. 6. In conclusion, chronic vitamin E deficiency imp airs 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 art ery. Sensorimotor nerves appear to be more vulnerable than sympathetic nerves to chronic vitamin E deficiency.