Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.11.11 (AMPK)
 12,425 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The rates of glycolysis and glycogenolysis an the rate of lactate formation from glucoso-6-phosphate (G-6-Ph) in the liver were reduced during stress (starvation). On the contrary, these activities in the adrenals were increased. The rates of lactate formation from fructose diphosphate remained unchanged in both organs. The results obtained attest to the inhibition in the liver and activation in the adrenals of phosphorylase, hexokinase and phosphofructokinase. The degree of hexokinase inhibition in the liver depended on the presence of cAMP, ATP and MgCl2 in the incubation medium and was a consequence of enzymatic phosphorylation. Unlike 2', 3'-AMP, the inhibitory effect of CAMP was highly specific. The protein inhibitor of protein kinase completely reversed the inhibitory effect of cAMP on hexokinase. In the adrenals, cAMP slightly increased the rates of glycolysis and lactate formation from G-6-Ph because of allosteric effects of cAMP. The activation rather than inhibition of glycolysis in the adrenals during stress is probably caused by the absence in this tissue of cAMP-dependent protein kinase which phosphorylates hexokinase.
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PMID:[Effect of cAMP of glycolysis and glycogenolysis in the liver and adrenals of white rats]. 627 Dec 95

We studied how extracellular cyclic AMP (cAMP) dilates the isolated and perfused canine coronary artery using pharmacological tools. Single injections of cAMP (1-1000 nmol), adenosine 3',5'-cyclic monophosphorothioate Sp-isomer (Sp-cAMPS) (10-1000 nmol, an agonist of the cell surface cAMP receptor in Dictyostelium discoideum and of cAMP-dependent protein kinase), adenosine (0.1-1000 nmol) and 5'-AMP (0.1-1000 nmol) dilated the canine coronary artery dose dependently. The potency order for vasodilation was adenosine > 5'-AMP > cAMP > Sp-cAMPS > 8-bromo-cyclic GMP > 3'-AMP > 8-bromo-cAMP > N6,O2'-dibutyryl-cAMP. 2'-Deoxy-cAMP, 2',3'-cAMP, guanosine, cGMP, 3'-GMP and 5'-GMP did not produce vasodilation. Adenosine antagonists such as aminophylline (1-100 microM, nonselective), 8-phenyltheophylline (0.1-10 microM, A1 selective), 8-cyclopentyl-1,3-dipropylxanthine (0.01-1 microM, A1 selective) and 3,7-dimethyl-1-proparglyxanthine (0.01-1 microM, A2 selective) shifted the dose-response curve of adenosine in parallel to the right, but they shifted that of cAMP to the right and downwards. 8-Phenyltheophylline (1 and 10 microM) inhibited the response to Sp-cAMPS (100 nmol) dose dependently. Aminophylline (10 microM) did not affect isoproterenol- and forskolin-induced vasodilations. Adenosine deaminase (3 U/ml) completely inhibited the response to adenosine, but not those to 5'-AMP, cAMP, 8-bromo-cAMP and Sp-cAMPS. 5'-Nucleotidase inhibitors, adenosine-5'-(alpha,beta-methylene) diphosphate (10 microM) and 5'-GMP (1 mM), inhibited the responses to cAMP and 5'-AMP, but not that to adenosine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pharmacological analysis of vasodilation induced by extracellular adenosine 3',5'-cyclic monophosphate in the isolated and perfused canine coronary artery. 838 43