Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:4.6.1.1 (adenylate cyclase)
 19,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the present work was to explain the mechanism of the stimulating effect of adrenaline (A) on acetylcholine (ACh) synthesis. This action is exerted most probably through the beta- adrenergic receptors, since propranolol and oxprenolol inhibit the stimulating effect of adrenaline on acetylcholine synthesis in the rat cerebral cortex in vitro. Dihydroergotamine does not show such effect. Practolol and phentolamine decrease the spontaneous synthesis of ACh in concentration several times lower than that inhibiting the ACh synthesis stimulated by adrenaline. It is suggested that adrenaline-induced stimulation of ACh synthesis in the rat cerebral cortex is not due to cyclic AMP, because noradrenaline (NA) does not increase ACh synthesis either in vivo or in vitro, although it activates the adenyl cyclase. NA on the other hand activates ACh synthesis in the calcium-free medium, which inhibits activating effect of NA on adenyl cyclase. Moreover it was found that cyclic AMP depresses ACh synthesis in the rat cerebral cortex in vitro.
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PMID:The effect of adrenaline on acetylcholine synthesis after blockade of alpha- and beta-adrenergic receptors in vitro. 2 84

Epinephrine infusion, 5-percent oxygen breathing, and splenic nerve stimulation were employed to increase cardiac output by 50-100% in anesthetized dogs. Epinephrine infusion as expected, increased plasma and myocardial cyclic AMP concentrations. Arterial hypoxemia increased cyclic AMP concentration in plasma but not in the heart. Practolol pretreatment abolished the increase in plasma cyclic AMP concentration and reduced the rise in cardiac output during hypoxemia. Splenic nerve stimulation was not associated with increases in either plasma or myocardial cyclic AMP. Adenylate cyclase activity was increased by addition of plasma into the incubation medium. However, splenic venous plasma obtained during splenic nerve stimulation did not increase adenylate cyclase activity more than control plasma obtained before stimulation. We conclude that the positive inotropic action of arterial hypoxemia and splenic nerve stimulation does not depend on the adenylate cyclase-cyclic AMP system.
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PMID:Effects of arterial hypoxemia and splenic nerve stimulation on myocardial adenosine 3',5'-Monophosphate in dogs. 16 96