1,720,971 research outputs found
Beta-adrenergic receptor regulation of a cyclic nucleotide phosphodiesterase in C6 glioma cells
No full textRegulation of intracellular and nuclear metabolism by stimulation of beta-adrenergic receptors on C6 glioma cells
No full textDopaminergic modulation of adenylate cyclase stimulated by vasoactive intestinal peptide in male rat anterior pituitary
No full textDopaminergic modulation of adenylate cyclase stimulation by vasoactive intestinal peptide in anterior pituitary
No full textBeta-adrenergic regulation of a Ca++-independent cAMP specific cyclic nucleotide phosphodiesterase in C6 glioma cells.
No full textInvolvement of a high-affinity GTPase in the inhibitory coupling of striatal muscarinic receptors to adenylate cyclase
No full textThe stimulation of GTP hydrolysis has been proposed as a mechanism by which hormones inhibit receptor-coupled adenylate cyclase activity. The present study attempts to verify whether this mechanism is also operative in transmitter-mediated receptor-coupled attenuation of adenylate cyclase [ATP pyrophosphate-lyase (cyclizing), EC 4.6.1.1] located in synaptic plasma membrane preparations. As a model, we used the inhibition of adenylate cyclase activity by muscarinic receptor activation in rat striatum. This striatal preparation contains high-affinity GTPase (EC 3.6.1-) activity which is stimulated when the recognition site for muscarinic agonists is occupied. Acetylcholine (ACh), but not nicotine, increases the Vmax of the high-affinity GTPase, and the stimulatory effect is antagonized by atropine but not by d-tubocurarine. The rank order of potency of various cholinergic agonists to stimulate GTPase correlates with their ability to inhibit adenylate cyclase activity of striatal membranes. Pre-exposure of striatal membranes to guanosine-5'-O-(3-thiotriphosphate) causes a parallel decrease in the basal and ACh-stimulated GTPase activities and in the ACh-induced inhibition of adenylate cyclase. Treatment of the membranes with cholera toxin does not affect the ACh-stimulated GTPase activity but amplifies the extent of adenylate cyclase inhibition elicited by the cholinergic agonist. These results indicate that the stimulation of a high-affinity GTPase parallels the inhibitory coupling of central muscarinic receptors to adenylate cyclase
Regulation by a beta-adrenergic receptor of a Ca2+-independent adenosine 3',5'-(cyclic)monophosphate phosphodiesterase in C6 glioma cells
No full textInhibitory coupling of dopamine receptors to adenylate cyclase in rat anterior pituitary
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