vasoactive-intestinal-peptide and Alcoholism

To determine whether chronic alcoholism alters the expression levels of Vasoactive intestinal polypeptide (VIP) and its receptor (VIPR1) in the cochlea of chronic alcoholism rats.. We measured their expression levels in 30 SD rats, in which we created models of different degrees of chronic alcoholism. We investigated the presence of the mRNA of VIP in the cochlea of chronic alcoholism rats and controls by reverse transcription-polymerase chain reaction (RT-PCR) method. We investigated the presence of proteins of VIPR1 in poisoned rats and controls by western blot. We also evaluated the local distribution of VIP cells by immunohistochemistry.. We found that the levels of VIP and VIPR1 were downregulated in the chronic alcoholism groups compared to the controls group. The differences in some expression levels were significant different between chronic alcoholism rats and control rats. Moreover, at different degrees of alcohol poisoning in rats, the contents of VIP and VIPR1 differed. Decreased levels of VIP and VIPR1 were detected in the deep chronic alcoholism group compared to the group with low-degree poisoning (P < 0.05). In spiral ganglion cell plasm the expression of VIP and VIPR1 had no significant difference in three groups (P > 0.05).. These results suggest that VIP and VIPR1 play an important role in the auditory function in rats with chronic alcoholism. Chronic alcoholism may cause a peptide hormone secretion imbalance in the auditory system, eventually leading to hearing loss.

Topics: Alcoholism; Animals; Cochlea; Disease Models, Animal; Down-Regulation; Rats; Rats, Sprague-Dawley; Receptors, Vasoactive Intestinal Polypeptide, Type I; RNA, Messenger; Spiral Ganglion; Vasoactive Intestinal Peptide

The possibility that long-term ethanol ingestion might alter either vasoactive intestinal peptide (VIP) content, VIP binding to membrane receptors, G-protein levels or adenylate cyclase activity in rat prostate was tested, as ethanol produces serious alterations in the hypothalamic-pituitary-gonadal axis and several modifications on different elements on signal transduction pathways in other systems.. Prostatic membranes from control and ethanol-treated (for 4 weeks) rats were used to study adenylate cyclase stimulation as well as for the immunodetection of stimulatory (alpha(s)) and inhibitory (alpha(i)1-2) G-protein subunits. Studies on VIP binding and cross-linking to receptors were performed using [125I]VIP. Prostatic VIP content was estimated by radioimmunoassay. GTPase activity was quantified by measuring the amount of 32Pi released from [gamma-32P]GTP.. Chronic ethanol ingestion resulted in an increased presence of VIP in the rat prostate without any change on the VIP receptor/effector system in this gland. By contrast, the basal adenylate cyclase activity as well as the dose-dependent stimulation of this enzyme by either the nonhydrolyzable GTP analogue Gpp(NH)p or the beta-adrenergic agonist isoproterenol were enhanced in prostatic membranes after ethanol intake. Moreover, an increase in the content of G-protein subunits (alpha(S) and alpha(i)1-2) was observed without any change in GTPase activity in this condition. These modifications were accompanied by a significant decrease in rat prostate weight and, consequently, the height of the secretory epithelium in this gland.. Considering the role of VIP in the mechanisms of secretion and cell proliferation in the prostate, the observed increases in the prostatic content of VIP and G-protein subunits make conceivable that VIP and cAMP signal transduction could be involved in the atrophy of the rat prostate and in the alterations in the composition of seminal fluid that appear in the alcoholic syndrome.

Topics: Adenylyl Cyclases; Alcoholism; Animals; Atrophy; Colforsin; Cyclic AMP; Enzyme Activation; Ethanol; GTP Phosphohydrolases; GTP-Binding Proteins; Guanylyl Imidodiphosphate; In Vitro Techniques; Male; Prostate; Protein Conformation; Rats; Rats, Wistar; Receptors, Vasoactive Intestinal Peptide; Signal Transduction; Vasoactive Intestinal Peptide

These results provide morphological evidence for an alcohol-induced selective intrapancreatic nerve degeneration. This affected mainly the nerve fibers that are inhibitory of the exocrine pancreas, and might represent the morphological background of hypersecretory state of the pancreas in chronic alcoholism.. Intrapancreatic intrinsic nerves were studied by immunohistochemistry and electron microscopy after 4 mo of alcohol consumption and compared with control mice.. A dense network of nerve fibers was observed in the normal mouse pancreas around the blood vessels and ending on the exocrine cells. The presence of VIP, NPY, PP, SP, and serotonin in these nerves was demonstrated by immunohistochemistry. Four months of alcohol consumption did not result in apparent morphological changes of the pancreas. However, the majority of periacinar nerve terminals showed degenerative changes. Synaptic vesicles were diminished in number in some other nerve processes, whereas the perivascular nerve fibers were relatively well preserved. A slight decrease was found in the intensity of VIP and SP immunoreactivity, and the PP fibers almost disappeared.

Topics: Alcoholism; Animals; Ethanol; Immunohistochemistry; Male; Mice; Microscopy, Electron; Nerve Degeneration; Nerve Endings; Nerve Fibers; Pancreas; Pancreatic Polypeptide; Synaptic Vesicles; Vasoactive Intestinal Peptide

Histochemical, immunohistochemical and neurochemical techniques were used to examine the innervation of epineurial nerve sheaths and fascicular nerve bundles of human sural and optic nerves from controls and patients with peripheral neuropathy due to diabetes or alcoholism. The normal distribution of autonomic nerves in both nerve trunk sheaths consisted of a dense innervation by noradrenaline (NA)-containing nerves of the vasa nervorum, together with some fibres in the nervi nervorum. Intrafascicular NA-containing nerves were only present in the sural nerve. Vasoactive intestinal polypeptide (VIP)- and neuropeptide Y (NPY)-containing nerves also innervated the vasa nervorum and nervi nervorum of the nerve sheaths, although their density was considerably less. Substance P (SP)-containing nerves were sparse and primarily intrafascicular. Neurochemical assays for NA, VIP, NPY and SP in fascicular and epineurial preparations from the sural and optic nerves confirmed the light microscopical observations. Post mortem delay significantly affected the NA levels in the sural nerve but not in the optic nerve while the NA fascicular/epineurial ratio for the sural nerve was independent of this factor. Age, sex and the presence of alcohol at time of death had no effect on transmitter levels in normal sural nerves. In the optic nerve fascicles NA levels were higher in females than in males. In patients with peripheral neuropathy there was a significant reduction in the SP fascicular/epineurial ratio in both the optic nerve, which was histologically normal, and in the sural nerve, where there was evidence of neuropathy. The NA fascicular/epineurial ratio was also significantly reduced in the sural nerve from patients with peripheral neuropathy with a possible greater effect in diabetes.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Aged; Alcoholism; Autopsy; Diabetes Mellitus; Female; Histocytochemistry; Humans; Immunohistochemistry; Male; Middle Aged; Nerve Fibers, Myelinated; Neuropeptide Y; Neuropeptides; Norepinephrine; Optic Nerve; Substance P; Sural Nerve; Vasoactive Intestinal Peptide

1. The effect of chronic intake of ethanol on the binding of vasoactive intestinal peptide (VIP) to rat spleen lymphoid cells was investigated. 2. The intake chronic of ethanol elicited an increase in specific VIP binding. 3. This increase was due to an increase in binding capacity of both the high and the low affinity binding sites. 4. There was a decrease in the affinities of both classes of VIP binding sites.

Topics: Alcoholism; Animals; Ethanol; In Vitro Techniques; Iodine Radioisotopes; Kinetics; Lymphoid Tissue; Rats; Rats, Inbred Strains; Spleen; Vasoactive Intestinal Peptide

The colonic cyclic AMP system is known to be involved in intestinal secretion and can be stimulated by a variety of gastrointestinal hormones including prostaglandins. We have investigated the effect of chronic ethanol ingestion on the activity of the key enzymes in cyclic AMP metabolism--adenylate cyclase and cyclic AMP phosphodiesterase--in the colonic mucosa of the rat. Chronic ethanol consumption by feeding a nutritionally adequate liquid diet enhanced basal colonic adenylate cyclase activity significantly by 168% (p less than 0.01), but had no effect on colonic low Km cyclic AMP phosphodiesterase activity. In addition, various hormonal secretagogues were used to stimulate colonic adenylate cyclase. Colonic adenylate cyclase exhibited a significantly greater sensitivity and efficacy to prostaglandins and vasoactive intestinal peptide after chronic ethanol ingestion. Since increased intestinal cyclic AMP production due to an increased activity of intestinal adenylate cyclase is known to promote intestinal secretion of water and electrolytes, the frequently observed diarrhea in alcoholics may be explained at least in part by an enhanced production of colonic cyclic AMP.

Topics: 3',5'-Cyclic-AMP Phosphodiesterases; Adenylyl Cyclases; Alcoholism; Animals; Colon; Cyclic AMP; Dinoprostone; Epoprostenol; Gastrointestinal Hormones; Humans; Intestinal Mucosa; Male; Prostaglandins E; Rats; Rats, Inbred Strains; Vasoactive Intestinal Peptide

Chronic ethanol consumption significantly increases gastric adenylate cyclase (AC) activity (p less than 0.05) without influencing low Km 3',5'-cyclic adenosine monophosphate (cAMP) phosphodiesterase (PD) activity in the rat. On the other hand, in the duodenum and upper part of the jejunum, chronic ethanol feeding leads to a significant decrease of adenylate cyclase activity (p less than 0.02) and, again, does not affect low Km cAMP phosphodiesterase activity. In addition, the effect of various hormonal secretagoques on small intestinal adenylate cyclase activity was investigated. Prostaglandin I2 and D2, as well as glucagon, do not stimulate AC at all. However, small intestinal adenylate cyclase exhibits a lower sensitivity to prostaglandin E2 and vasoactive intestinal peptide (VIP), and a lower efficacy to VIP after chronic ethanol consumption when compared to controls. The decrease of both basal and stimulated AC activity following ethanol ingestion in the upper small intestine may be due to membrane alterations and tissue damage caused by ethanol. The ethanol-induced increase in gastric AC may be of relevance with respect to an increased acid secretion observed after alcohol administration.

Topics: 3',5'-Cyclic-AMP Phosphodiesterases; Adenylyl Cyclases; Alcoholism; Animals; Cyclic AMP; Dinoprostone; Gastric Mucosa; Humans; Intestinal Mucosa; Intestine, Small; Kinetics; Male; Prostaglandins E; Rats; Rats, Inbred Strains; Vasoactive Intestinal Peptide