Effects of Alcohols on the Actions of VIP and Secretin on Acinar Cells from Guinea Pig Pancreas

Uhlemann, Edward R.; Robberecht, Patrick; Gardner, Jerry D.

doi:10.1016/s0016-5085(79)91318-0

Cited by 47 publications

(13 citation statements)

References 44 publications

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“…Also in these studies with cholinergic agonists the exact location of the alcohol ') To whom correspondence should be directed. effect remains speculative, but assumptions of the role of the muscarinic receptors have been stated in several studies (Perec et al 1979;Uhlemann et al 1979;Kubota et al 1983;Schmidt 1984).…”

mentioning

confidence: 99%

Decrease in the Number of Muscarinic Receptors in Rat Pancreas after Chronic Alcohol Intake

Grönroos

Kaila

Aho

et al. 1989

Pharmacology & Toxicology

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The effect of eight months of alcohol intake on the number and affinity of muscarinic receptor sites in the rat pancreatic tissue were measured by using N-3H-methylscopolamine (NMS) as a radioligand. There were no differences in the receptor affinities for NMS between the alcohol-exposed and age-matched control animals, but the number of muscarinic receptor sites was 60 percent lower in the alcoholic animals. The present experimental model is consistent with altered food and water intake as consequences of chronic alcoholism and thus changes in food and water consumption may participate in mediating the effects of chronic alcohol intake on NMS binding sites. We suggest that the previously reported marked alcohol-induced increase in pancreatic acetylcholine levels, which has been proposed to play a crucial role in the pathogenesis of acute alcoholic pancreatitis, may be a secondary phenomenon induced by increased resistance at the muscarinic receptor level.

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confidence: 99%

Decrease in the Number of Muscarinic Receptors in Rat Pancreas after Chronic Alcohol Intake

Grönroos

Kaila

Aho

et al. 1989

Pharmacology & Toxicology

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“…Adenylate cyclase (AC) activity in peripheral organs (Gorman and Bitensky, 1970;Uhlemann et al, 1979), as well as in the CNS Molinoff, 1981, 1983;Luthin and Tabakoff, 1984;Saito et al, 1985), can be stimulated by ethanol. Recently, specific sites of action for ethanol in some of these systems have been described by Rabin and Molinoff (1983) and by Luthin and Tabakoff (1984).…”

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confidence: 99%

Effects of Chronic Ethanol Treatment on the β‐Adrenergic Receptor‐Coupled Adenylate Cyclase System of Mouse Cerebral Cortex

Saito

Lee

Hoffman

et al. 1987

Journal of Neurochemistry

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Chronic ingestion of ethanol, which produced tolerance and physical dependence, resulted in altered function of the cerebral cortical beta-adrenergic receptor-coupled adenylate cyclase system in mice. Although there was no change in basal adenylate cyclase activity, or in the activity of the digitonin-solubilized catalytic unit, stimulation of adenylate cyclase activity by the nonhydrolyzable guanine nucleotide analog guanylylimidodiphosphate [Gpp(NH)p] was reduced in brains of ethanol-fed animals. Ethanol added in vitro increased adenylate cyclase activity, and this enhancement, in the presence of Gpp(NH)p, was also reduced in cortical membranes of ethanol-fed mice. Furthermore, the maximal response to isoproterenol was decreased, and the EC50 for isoproterenol stimulation of adenylate cyclase activity was increased in ethanol-fed animals. The results are consistent with a qualitative or quantitative defect in the function of the stimulatory guanine nucleotide-binding protein (Ns), as well as in the beta-adrenergic receptor, after chronic ethanol exposure. In part, these changes appear to be similar to those that occur during heterologous desensitization of various receptor systems, and may be associated with dependence on or tolerance to ethanol.

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“…The response of membrane-bound enzyme systems to membrane perturbations cannot, however, be predicted with certainty. For instance, equimolar concentrations of ethanol inhibit Na-K/ATPase activity (Hoyumpa et al, 1977), but stimulate adenylate cyclase (AC) ac-tivity in membranes of a number of peripheral organs (Gorman and Bitensky, 1970;Uhlemann et al, 1979;Whetton et al, 1983).…”

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confidence: 99%

“…AC plays a major role in regulating intracellular levels of cyclic AMP and generating intracellular messages in response to extracellular stimuli. Although certain of the earlier studies (Gorman and Bitensky, 1970;Uhlemann et al, 1979) have provided evidence for a lipid locus for ethanol's effects on AC activity, these early studies of ethanol's effects on hormone-stimulated AC in peripheral organs paid little attention to the various factors (i.e., guanine nucleotides and magnesium) now known to regulate AC activity.…”

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confidence: 99%

Ethanol's Effects on Cortical Adenylate Cyclase Activity

Saito

Lee

Tabakoff

1985

Journal of Neurochemistry

111

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The effects of ethanol on beta-adrenergic receptor-coupled adenylate cyclase (AC) of mouse cerebral cortex were examined. The addition of ethanol (20-500 mM) to incubation mixtures containing cortical membranes demonstrated that ethanol could increase AC activity and potentiate the stimulatory effects of guanylyl-imidodiphosphate [Gpp(NH)p] on AC activity. Ethanol increased the rate of activation of AC by guanine nucleotides and concomitantly decreased the EC50 for magnesium required to achieve maximal stimulation of cortical AC. The EC50 values for Gpp(NH)p and isoproterenol stimulation of AC activity were also altered by ethanol. Ethanol was capable of stimulating AC extracted by use of digitonin. The AC activity in the digitonin extract was no longer sensitive to the addition of Gpp(NH)p or NaF, but was still stimulated by ethanol. We propose multiple sites of action for ethanol in stimulating cortical AC activity. These sites include actions at the beta-adrenergic receptor, at the G/F coupling proteins, and at the catalytic unit of cortical AC. Comparison of ethanol's actions on cortical beta receptor coupled AC activity with prior reported actions of ethanol on striatal dopamine (DA)-sensitive AC indicated differential sensitivities of these two AC systems to ethanol. These differences may be determined by specific coupling characteristics of the striatal and cortical AC systems or by differences in the plasma membranes in which striatal and cortical AC systems are located.

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Effects of Alcohols on the Actions of VIP and Secretin on Acinar Cells from Guinea Pig Pancreas

Cited by 47 publications

References 44 publications

Decrease in the Number of Muscarinic Receptors in Rat Pancreas after Chronic Alcohol Intake

Decrease in the Number of Muscarinic Receptors in Rat Pancreas after Chronic Alcohol Intake

Effects of Chronic Ethanol Treatment on the β‐Adrenergic Receptor‐Coupled Adenylate Cyclase System of Mouse Cerebral Cortex

Ethanol's Effects on Cortical Adenylate Cyclase Activity

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