Effects of vitamin E deficiency on autonomic neuroeffector mechanisms in the rat caecum, vas deferens and urinary bladder.

Abstract

1. Modified sucrose-gap, standard organ-bath techniques and transmitter release studies were used to examine neuromuscular transmission in the caecum, vas deferens and urinary bladder in normal rats and in rats maintained for 12 months on a diet free of vitamin E. 2. In the caecum circular muscle, non-adrenergic, non-cholinergic inhibitory junction potentials were absent from 48 and 15 % of preparations from vitamin E-deficient and control animals, respectively. Cholinergic excitatory junction potentials were absent from 83 and 8 % of vitamin E-deficient and control preparations, respectively. Responses to applied noradrenaline (0 1-30 uM), a,f-methylene ATP (3-100 ZM) and acetylcholine (0 1-30 #M)were attenuated or absent in vitamin E-deficient tissues. Responses to applied KCI were similar in both groups. Release of [3H]noradrenaline or endogenous acetylcholine could not be evoked from vitamin E-deficient tissues. 3. In contrast, in isolated preparations of the vas deferens and urinary bladder, neuromuscular transmission by adrenergic, cholinergic and purinergic components were unaffected by long-term vitamin E deficiency. 4. In conclusion, vitamin E deficiency causes dysfunction of autonomic neuroeffector mechanisms in the smooth muscle of the rat caecum, at both a pre-and postjunctional level. The lesions in autonomic transmission mechanisms brought about by long-term vitamin E deficiency were found only in the caecum; no changes in sympathetic neuromuscular transmission were observed in the vas deferens, or in parasympathetic neuromuscular transmission in the urinary bladder.It has become established that vitamin E (a-tocopherol) is essential for normal neuronal physiology, and that deficiency of vitamin E results in neuropathic changes (for reviews see

Effects of chronic vitamin E deficiency on vascular function ‐ a study of sympathetic nerves, smooth muscle and endothelium of the mesenteric arterial bed of the rat

“…However, there was no such increase in the frequency of neuroaxonal dystrophy in the coeliac/superior mesenteric sympathetic ganglia (Schmidt et al, 1991). A recent study showed that after 12 months of vitamin E deficiency there was dysfunction of non-adrenergic, non-cholinergic pre-and postjunctional autonomic transmission in the rat caecum, but no changes in sympathetic neuromuscular transmission in the rat urinary bladder (Hoyle et al, 1995), suggesting that the autonomic neuropathy is not a generalized process. In addition to NA, transmitters such as ATP and neuropeptide Y (NPY) are known to be coreleased from sympathetic nerves, particularly at high frequencies of stimulation (Burnstock, 1990), and it is possible that the relative proportions of these transmitters may change in vitamin E deficiency.…”

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

“…This is consistent with the results of a previous study reporting no changes in contractile responses to KCl and calcium in isolated segments of rat mesenteric arteries after vitamin E deficiency (Hubel et al 1989). Resistance of sympathetic transmission mechanisms to adverse effects of vitamin E deficiency also occurs in the vas deferens, at a time when enteric transmission (both cholinergic and purinergic) is distinctly impaired (Hoyle et al 1995).…”

Gene expression analysis of neuropeptides in oral mucosa during periodontal disease in non‐human primates

“…In particular, peptide neurotransmitters produce actions on extracellular receptors of target cells including neural and non-neural cells such as macrophages, lymphocytes, and endothelial cells. 7–9 …”

“…6 In particular, peptide neurotransmitters produce actions on extracellular receptors of target cells including neural and non-neural cells such as macrophages, lymphocytes, and endothelial cells. [7][8][9] Accordingly, differential modulation of cytokine production by NPs has been shown in several immune cell types, including antigen-presenting cells as well as B and T cells. 6,10 In addition to their immunoregulatory role, some NPs (e.g., calcitonin gene-related peptide [CGRP]) have also been shown to be involved in bone metabolism directly affecting osteoblast and osteoclast function through receptor activation, or indirectly enhancing production of pro-inflammatory cytokines.…”