Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Basal adenosine 3',5'-cyclic monophosphate (cAMP) content and the modulation of its production were studied in the frog's semicircular canal epithelium. This epithelium secretes endolymph, a K(+)-rich, positively polarized fluid. The basal cAMP content measured by microradioimmunoassay was 244 +/- 14.2 fmol/structure per 5 min (n = 30). This content was increased about 8 times by 10(-5) M forskolin. Vasotocin, the frog antidiuretic hormone, increased the cAMP production by factors of 1.3 and 3.3 at concentrations of 10(-8) M and 10(-7) M, respectively. This stimulatory effect of vasotocin was blunted by the addition of alpha 2-adrenergic agonists, such as 10(-8) M-10(-5) M norepinephrine, in the presence of 10(-5) M propranolol, or 10(-5) M clonidine. Prostaglandin E2 at a concentration of 10(-8) M, which did not affect the cAMP production, did not modify the response to vasotocin. Glucagon (10(-6) M), calcitonin (10(-6) M), and parathyroid hormone (10 units/ml) did not affect the cAMP content. Prostaglandin E2 (10(-7) M) and the beta-adrenergic agonist isoproterenol (10(-6) M) stimulated the cAMP production by a factor of 1.6. These results indicate that the frog semicircular canal is a target of both vasotocin and catecholamines and that catecholamines through alpha 2-receptors modulate vasotocin-induced cAMP generation. Further, this interaction might be of physiological relevance in the modulation of ion transport in this structure.
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PMID:Antidiuretic hormone stimulation of adenylate cyclase in semicircular canal epithelium. 167 38

Arginine vasotocin (AVT) and isotocin (IT) induced direct inhibition of adenylate cyclase activity in gill plasma membranes of the rainbow trout adapted to freshwater (FW) and seawater (SW). The maximal inhibition was obtained with 10(-11)-10(-10) M (50% inhibitory concentration approximately 10(-13) M), values in agreement with the circulating levels of AVT in trout blood. Specific V1 or V2 agonists or antagonists (with reference to vasopressin) were used to define the specificity of the neurohypophysial peptide receptors involved in this inhibition. The V1 agonist [Phe2,Orn8]vasotocin ([Phe2]OVT) inhibited the basal and glucagon-stimulated adenylate cyclase activity, and this effect in SW (20%) was twice more than in FW (10%). The V2 agonist 1-deamino[Val4,Arg8]-vasopressin (dVDAVP), however, produced a stimulation that was of the same amplitude (10%) in both media. The V1 antagonist [(1-beta-mercapto-beta-beta-cyclopentamethylenepropionic acid), 1-(O-ethyl)Tyr2,Orn8]vasotocin (d(CH2)5[Tyr(Et)2]OVT) totally reversed the AVT- or IT-induced inhibition of basal or glucagon-stimulated cyclase activity, whereas the V1/V2 antagonist [(1-beta-mercapto-beta-beta-cyclopentamethylene propionic acid), 1-(O-ethyl)D-Tyr2,Val4,Arg8]vasopressin (d(CH2)5[D-Tyr(Et)2]-VAVP) (previously used as V2 antagonist in amphibians) had no such effect. When active, all analogues had their maximal activity at 10(-11)-10(-10) M (50% maximal activity approximately 10(-13) M), as observed with the natural peptides. These results, together with our previous observations, point to the gill epithelium as a direct target organ for neurohypophysial peptides and suggest that the hormone receptors involved in fish belong predominantly, if not exclusively, to a new type that we propose to designate as fish neurohypophysial hormone (NHF) receptors while awaiting further characterization.
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PMID:Evidence for presence of a new type of neurohypophysial hormone receptor in fish gill epithelium. 230 44

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 5x10(-8) M glucagon (maximal effect for 4.5x10(-7) M and 1.4x10(-7) M, half-maximal effect for 2.1x10(-8) M and 0.7x10(-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 V(1) agonist [Phe(2), Orn(8)]-oxytocin inhibited the glucagon-stimulated cAMP production with a maximal effect for 6x10(-7) M and a half-maximal effect for 0.9x10(-8) M concentrations of the analogue. While the V(1) agonist reduced the glucagon-stimulated cAMP level by 70%, it showed only a tendency to reduce the basal level. The V(2) agonist [deamino(1), Val(4),d -Arg(8)]-vasopressin had no effect either on basal or on glucagon-stimulated cAMP production. The V(1) antagonist [d(CH(2))(5)(1), O-Me-Tyr(2), Arg(8)]-vasopressin totally reversed the 10(-8) M AVT-induced inhibition of 5x10(-8) M glucagon-stimulated cAMP production, whereas the V(2) antagonist [d(CH(2))(5)(1),d -Ile(2), Ile(4), Arg(8), Ala(9)]-vasopressin had no such effect. In this particular case, maximal and half-maximal effects of the V(1) antagonist were obtained for 2.3x10(-6) M and 1. 2x10(-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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PMID:Neurohypophysial hormone receptors and second messengers in trout hepatocytes. 1101 61