Studies on the mechanism of inhibition of hepatic cAMP accumulation by vasopressin

Morgan, Noel G.; Shipp, Clanton C.; Exton, John H.

doi:10.1016/0014-5793(83)80835-7

Cited by 27 publications

(14 citation statements)

References 21 publications

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“…Glucagon secretion could be increased by VP through activation of V1bR in pancreatic islets [7][8][9], or indirectly by stimulating adrenaline (epinephrine) secretion by chromaffin cells of the adrenal medulla [36]. Crosstalk between V1aR and glucagon receptor and their signalling pathways has been described also in hepatocytes [37,38]. However, glucagon is not likely to play a role in the disturbances of glucose metabolism observed in the present study because basal plasma glucagon concentration and glucagon response during ITT were unaltered by chronic VP treatment.…”

Section: Discussionmentioning

confidence: 99%

Vasopressin and hydration play a major role in the development of glucose intolerance and hepatic steatosis in obese rats

et al. 2015

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Aims/hypothesis High plasma copeptin, a marker of vasopressin (VP) secretion, has been shown to be associated with the metabolic syndrome and development of type 2 diabetes in humans. The present study was designed to determine the long-term influence of plasma VP concentration in a rodent model prone to metabolic dysfunction. Methods Obese Zucker rats and their lean counterparts were submitted for 4 weeks to one of three protocols inducing different levels of VP. Circulating VP was either reduced by increasing the daily water intake (low-VP), or increased by a chronic i.p. infusion of VP (high-VP). The control rats had normal VP levels that depended on their own regulation of water intake and VP secretion.Results Compared with controls with normal VP, lean rats with high-VP had a higher fasting glycaemia after 4 weeks. In obese rats, high-VP promoted hyperinsulinaemia, glucose intolerance, assessed by glucose and insulin tolerance tests, and an impaired response to a pyruvate challenge. Conversely, treatment with a selective arginine vasopressin receptor 1A (V1aR) antagonist reduced glucose intolerance. Low-VP obese rats had unchanged glucose tolerance but exhibited a drastic decrease in liver steatosis compared with control obese rats, associated with low hepatic triacylglycerol and cholesterol content, and reduced expression of hepatic lipogenic genes. These effects were independent of changes in body adiposity, and plasma sodium and osmolality did not differ among groups.Electronic supplementary material The online version of this article

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Section: Discussionmentioning

confidence: 99%

Vasopressin and hydration play a major role in the development of glucose intolerance and hepatic steatosis in obese rats

et al. 2015

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“…The stimulation by glucagon was decreased up to 90% by AVT and 80% by IT, for an AVT or IT concentration of 4·5 2·1 10 -7 M (n=7) and 1·4 1·0 10 -7 M (n=3), respectively. In rat liver, 10 -8 M vasopressin used in similar conditions was only able to reduce by 16% the cAMP accumulation induced by 10 -8 M glucagon (Morgan et al 1983). In rat brain, vasopressin was found partially to prevent the cAMP accumulation induced by noradrenaline, dopamine and forskolin (50%, 45% and 40% by 3 10 -7 , 5·5 10 -7 and 3 10 -7 M AVP respectively, Newman 1985).…”

Section: Discussionmentioning

confidence: 91%

“…The intervention of protein kinases leads to protein phosphorylation (Morris et al 1994) and to activation of mitogen-activated protein kinase (Romanelli & Van de Werve 1997). Another effect of vasopressin is to inhibit, in a dose-dependent manner, the cAMP accumulation induced by forskolin or glucagon whether cells are depleted in calcium or not (Morgan et al 1983).…”

Section: Introductionmentioning

confidence: 99%

Neurohypophysial hormone receptors and second messengers in trout hepatocytes

Guibbolini

Pierson²,

Lahlou³

2000

Journal of Endocrinology

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Neurohypophysial hormone receptors and second messengers were studied in trout (Oncorhynchus mykiss) hepatocytes. Arginine vasotocin (AVT) and isotocin (IT) elicited a concentration-dependent inhibition of cAMP accumulation in the presence of 5 10 -8 M glucagon (maximal effect for 4·5 10 -7 M and 1·4 10 -7 M, half-maximal effect for 2·1 10 -8 M and 0·7 10 -8 M, AVT and IT respectively). The effect of glucagon was inhibited up to 90% by AVT and 80% by IT. While AVT inhibited (up to 50%) the basal cAMP production, IT had no such action.Specific V 1 or V 2 analogues (with reference to vasopressin in mammals) were used for pharmacological characterization of the type of neurohypophysial hormone receptor involved in this inhibition. The ]-vasopressin had no such effect. In this particular case, maximal and half-maximal effects of the V 1 antagonist were obtained for 2·3 10 -6 M and 1·2 10 -6 M respectively.Changes in intracellular calcium content were measured using the fluorescent probe FURA-2/AM. AVT and IT elicited a concentration-dependent increase in Ca 2+ accumulation. The comparison of the effect of 10 -8 M agonists versus AVT showed the following order of potency: AVT=IT>V 1 agonist>V 2 agonist. The V 1 antagonist reversed the AVT-induced Ca 2+ accumulation whereas the V 2 antagonist had no such effect.These results are taken as evidence for the presence in trout hepatocytes of neurohypophysial hormone receptors functionally close to the V 1a -type linked to cAMP production and Ca 2+ mobilization.

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“…In rat hepatocytes, Morgan et al (1983) showed that forskolin-or glucagon-induced cAMP increase was reduced 16-30% by AVP, with a concentration of AVP inducing 50% of this inhibitory effect (IC50) of about 01 nmol/1. It has also been suggested that this effect is exerted directly on adenylate cyclase (Crane et al 1982;Morgan et al 1983) and does not involve calcium mobilization.…”

Section: Resultsmentioning

confidence: 99%

“…Conversely, specific binding to the V, (vascular type) receptors has been shown more recently to be linked to a decrease in cyclic AMP (cAMP) and/or to calcium mobilization in the cell and phosphoinositol breakdown. The second mechanism is shown, for example, by the effects of vasopressin on mammalian hepatocytes (Crane, Campanile & Garrison, 1982;Morgan, Shipp & Exton, 1983).…”

Section: Introductionmentioning

confidence: 98%

Inhibitory effect of neurohypophysial peptides on cyclic AMP accumulation by isolated hepatocytes of the trout

Lahlou¹,

Fossat²,

Porthé-Nibelle³

et al. 1988

Journal of Endocrinology

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Cyclic AMP levels were measured in freshly isolated hepatocytes of the rainbow trout. Compared with basal values, the average levels were increased up to 60 times in a dose-dependent manner either by mammalian glucagon (concentration range 1 nmol-1 mumol/l; dose giving half maximum response (EC50) 0.18 mumol/l) or by forskolin (concentration range 0.1-100 mumol/l; EC50 about 10 mumol/l). These stimulatory effects were partially inhibited by fish or mammalian neurohypophysial hormones used at relatively high concentrations (1-5 mumol/l). It is suggested that these results are evidence for the presence of V1-type receptors in fish hepatocytes. Together with previous results obtained with gills on the hormonal inhibition of adenylate cyclase activity, they suggest that teleost fish may possess only V1-type receptors (or two V1-related types), while the V2 receptors have evolved (or have become functional) in higher vertebrates.

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Studies on the mechanism of inhibition of hepatic cAMP accumulation by vasopressin

Cited by 27 publications

References 21 publications

Vasopressin and hydration play a major role in the development of glucose intolerance and hepatic steatosis in obese rats

Vasopressin and hydration play a major role in the development of glucose intolerance and hepatic steatosis in obese rats

Neurohypophysial hormone receptors and second messengers in trout hepatocytes

Inhibitory effect of neurohypophysial peptides on cyclic AMP accumulation by isolated hepatocytes of the trout

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