Big Chemical Encyclopedia

Chemical substances, components, reactions, process design ...

Articles Figures Tables About

Phosphodiesterase demonstration

Cheung, W. Y. (1970). Cyclic 3, 5 -nucleotide phosphodiesterase Demonstration of an activator. Biochem. Biophys. Res. Commun. 38, 533-538. [Pg.129]

The inotropic effects of these agents are not mediated via direct stimulation of -adrenergic receptors or indirectly by release of catecholamines, but by selective inhibition of cardiac cAMP phosphodiesterase (PDE) type III [25,35-40]. Recently, it has been demonstrated that the imidazole core is primarily responsible for PDE isozyme specificity, whereas the dihydropyri-dazinone moiety is responsible for inhibitory potency the phenylene moiety obviously acts mainly as a spacer [26]. A five-point model for positive inotropic activity of PDE III inhibitors has been elaborated [41]. [Pg.146]

Visuai disturbances Single oral doses of phosphodiesterase inhibitors have demonstrated transient, dose-related impairment of color discrimination (blue/green), with peak effects near the time of peak plasma levels. The findings were most evident 1 hour after administration, diminishing but still present 6 hours after administration. [Pg.649]

Cilostazol is a phosphodiesterase inhibitor that reduces platelet aggregation, vascular smooth muscle proliferation and also has vasodilatory effects. Earlier studies comparing cilostazol and aspirin to ticlodipine and aspirin identified no significant increase in the subacute stent thrombosis rate (21-23). Indeed, the latter has been supported by comparison of this combination to clopidogrel and aspirin (24). Two recent trials, however, have demonstrated that a much higher proportion of patients develop subacute stent thrombosis when taking cilostazol as compared with ticlodipine (25,26). The data from these trials are summarized in Table I. [Pg.526]

The above-described data show that CRF added to cells of the rat Intermediate lobe In culture causes a rapid stimulation of oe-MSH release and cyclic AMP accumulation, thus demonstrating a direct action of the peptide on pars intermedia cells (15). It is however difficult, using intact cells, to dissociate between increases in cyclic AMP levels due to stimulation of adenylate cyclase activity or to Inhibition of cyclic nucleotide phosphodiesterase or to a combination of both effects. Definitive proof of the role of adenylate cyclase In the action of CRF In the intermediate lobe of the pituitary gland is provided by the following findings of a CRF-lnduced stimulation of adenylate cyclase activity in homogenate of rat and bovine pars Intermedia cells. [Pg.65]

Alkaline phosphatase, acid phosphatase, 5 -nucleotidase, monoacyl hydrolase, ribonuclease, type 1 phosphodiesterase, adenosine triphosphatase, adenyl cyclase, glycosyl transferase, esterases and disaccharidase have been biochemically or cytochemically demonstrated in the tegument of various cestodes (152, 210, 250, 374, 491, 620, 624-626, 651, 718, 763, 776, 898). Several of these enzymes - phosphatases, 5 -nucleotidase and phosphodiesterase - probably have a digestive and/or absorptive function but the role of the others is uncertain. [Pg.119]

The level of cyclic AMP inside the cell is the balance between synthesis, breakdown and release. Increased intracellular levels of cyclic AMP can therefore also be obtained by inhibition of cyclic AMP metabolism with phosphodiesterase inhibitors. There are many reports of the use of these inhibitors to demonstrate increased steroidogenesis at submaximal (but not maximal) concentrations of LH, thus confirming the involvement of cyclic AMP. [Pg.164]

Other evidence for the involvement of a G-protein in the action of insulin has come from studies by Walaas and co-workers [104]. They have demonstrated that insulin stimulated the activity of a cyclic AMP-dependent protein kinase activity in sarcolemma membranes. As this effect of insulin was enhanced if micromolar concentrations of GTP-binding protein were present, they suggested that a guanine nucleotide regulatory protein was involved in the hormonal control of this kinase. Indeed, cholera toxin also appeared to obliterate this action of insulin, as it did the effect of insulin on liver adenylate cyclase and the peripheral plasma membrane cyclic AMP phosphodiesterase in liver. [Pg.339]

Forskolin stimulates die catalytic subunit of adenylyl cyclase directly, bypassing the G proteins, which makes forskolin a much used substance in experiments with elevated platelet cAMP-levels. A number of agents has been demonstrated to inhibit the cAMP phosphodiesterases in platelets, e.g. papaverine, dipyridamole and the methylxantines... [Pg.212]

Although phosphodiesterase is generally not found extracellularly, its location at the external surface of skeletal muscle was demonstrated by incubating frog muscles with labelled cyclic AMP [52]. [Pg.298]


See other pages where Phosphodiesterase demonstration is mentioned: [Pg.781]    [Pg.61]    [Pg.70]    [Pg.197]    [Pg.101]    [Pg.306]    [Pg.905]    [Pg.50]    [Pg.309]    [Pg.6]    [Pg.423]    [Pg.296]    [Pg.156]    [Pg.112]    [Pg.239]    [Pg.325]    [Pg.37]    [Pg.439]    [Pg.193]    [Pg.622]    [Pg.222]    [Pg.232]    [Pg.304]    [Pg.70]    [Pg.37]    [Pg.109]    [Pg.200]    [Pg.49]    [Pg.351]    [Pg.63]    [Pg.489]    [Pg.8]    [Pg.338]    [Pg.338]    [Pg.339]    [Pg.268]    [Pg.7]    [Pg.2038]    [Pg.8]    [Pg.244]    [Pg.589]   
See also in sourсe #XX -- [ Pg.138 ]




SEARCH



Demonstration

Demonstrators

Phosphodiesterase

Phosphodiesterases

© 2024 chempedia.info