Cyclic adenosine 3 , 5 -monophosphate, formation

Brattleboro homozygotes) had intact arginine vasopressin-dependent cyclic adenosine monophosphate generation. The activity of cyclic adenosine monophosphate phosphodiesterase was not affected in lithium-treated rats. Hence, it seems that the main cellular effect of lithium involves impairment of arginine vasopressin-sensitive adenylate cyclase and that this results in impairment of intracellular cyclic adenosine monophosphate formation. 

P2-Agonists cause airway smooth muscle relaxation by stimulating adenyl cyclase to increase the formation of cyclic adenosine monophosphate (cAMP). Other non-bronchodilator effects have been observed, such as improvement in mucociliary transport, but their significance is uncertain.11 P2-Agonists are available in inhalation, oral, and parenteral dosage forms the inhalation route is preferred because of fewer adverse effects. 

Dl-iike receptors activate the Gs transduction pathway, stimulating the production of adenylyl cyclase, which increases the formation of cyclic adenosine monophosphate (cAMP) and ultimately increases the activity of cAMP-dependent protein kinase (PKA). PKA activates DARPP-32 (dopamine and cyclic adenosine 3, 5 -monophosphate-regulated phosphoprotein, 32 kDa) via phosphorylation, permitting phospho-DARPP-32 to then inhibit protein phosphatase-1 (PP-1). The downstream effect of decreased PP-1 activity is an increase in the phosphorylation states of assorted downstream effector proteins regulating neurotransmitter... 

Selective sympathomimetics cause relaxation of bronchial smooth muscle and bronchodilation by stimulating the enzyme adenyl cyclase to increase the formation of cyclic adenosine monophosphate. They may also improve mucociliary clearance. 

To date, five subtypes of these receptors have been cloned. However, initial studies relied on the pharmacological effects of the muscarinic antagonist pirenzepine which was shown to block the effect of several muscarinic agonists. These receptors were termed Mi receptors to distinguish them from those receptors for which pirenzepine had only a low affinity and therefore failed to block the pharmacological response. These were termed M2 receptors. More recently, M3, M4 and M5 receptors have been identified which, like the Mi and M2 receptors occur in the brain. Recent studies have shown that Mi and M3 are located posts)maptically in the brain whereas the M2 and M4 receptors occur pres)maptically where they act as inhibitory autoreceptors that inhibit the release of acetylcholine. The M2 and M4 receptors are coupled to the inhibitory Gi protein which reduces the formation of cyclic adenosine monophosphate (cyclic AMP) within the neuron. By contrast, the Mi, M3 and M5 receptors are coupled to the stimulatory Gs protein which stimulates the intracellular hydrolysis of the phosphoinositide messenger within the neuron (see Figure 2.8). 

Five subtypes of dopamine receptors have been described they are the Dj-like and Dj-like receptor groups. All have seven transmembrane domains and are G protein-coupled. The Dj-receptor increases cyclic adenosine monophosphate (cAMP) formation by stimulation of dopamine-sensitive adenylyl cyclase it is located mainly in the putamen, nucleus accumbens, and olfactory tubercle. The other member of this family is the D5-receptor, which also increases cAMP but has a 10-fold greater affinity for dopamine and is found primarily in limbic regions. The therapeutic potency of antipsychotic drugs does not correlate with their affinity for binding to the Dj-receptor. 

Activation of Gs or Gi proteins results in stimulation or inhibition, respectively, of adenylyl cyclase which catalyses the formation of cyclic adenosine monophosphate (cAMP) from ATP The cAMP binds to protein kinase A (PKA), which mediates the diverse cellular effects of cAMP by phosphorylating substrate enzymes, thereby increasing their activity. Among the responses mediated by cAMP are increases in contraction of cardiac and skeletal muscle and glycogenolysis in the liver by adrenaline (epinephrine). Because a single activated receptor can cause the conversion of up to 100 inactive Gs proteins to the active form, and each of these results in the synthesis of several hundred cAMP molecules, there is a very considerable signal amplification. For example, adrenaline concentrations as low as 10-10 M can stimulate the release of glucose sufficient to increase... 

Antidiuretic hormone antagonists inhibit the effects of ADH in the collecting tubule. Conivaptan is a pharmacologic antagonist at Via and V2 receptors. Both lithium and demeclocycline appear to reduce the formation of cyclic adenosine monophosphate (cAMP) in response to ADH. 

Maintenance of adrenal cortex Promotes secretion of steroids, oxidative phosphorylation in adrenal cortex Mobilizes and increases oxidation of free fatty acid in adipose tissue Increases gluconeogenesis in liver increases cyclic adenosine monophosphate (AMP) in adrenal cortex Decreases urea formation in liver... 

Prostaglandin inhibition of gastric acid secretion by blocking the formation of cyclic adenosine monophosphate... 

PGI2 exerts its inhibitory activity by increasing cyclic adenosine monophosphate (cAMP) formation via adenylate cyclase, which stimulates phosphorylation of a cytoskeleton integrin protein-associated vasodilator-stimulated phosphoprotein (VASP), which prevents GPIIb Ilia activation (16). 

The Ga proteins can be classified on the basis of similarities in their amino acid sequences and coupling to effector proteins. The four major categories are Gas, Gai, Gaq, and Gall and these are responsible for activating different signaling pathways in cells. Gas and Gai stimulate and inhibit adenylate cyclase, respectively. Adenylate cyclase is an enzyme that catalyzes the formation of cyclic adenosine monophosphate (cAMP), an intracellular second messenger... 

Adenylate cyclase is considered as a second messenger that catalyzes the formation of cAMP (cyclic adenosine monophosphate) from ATP this results in alterations in intracellular cAMP levels that change the activity of certain enzymes—that is, enzymes that ultimately mediate many of the changes caused by the neurotransmitter. For example, there are protein kinases in the brain whose activity is dependent upon these cyclic nucleotides the presence or absence of cAMP alters the rate at which these kinases phosphorylate other proteins (using ATP as substrate). The phosphorylated products of these protein kinases are enzymes whose activity to effect certain reactions is thereby altered. One example of a reaction that is altered is the transport of cations (e.g., Na+, K+) by the enzyme adenosine triphosphatase (ATPase). 

The mechanism of the action of lithium on H2O transport lies at some point along the arginine vasopressin-mediated transport process, either before or beyond the formation of cyclic adenosine monophosphate. Forrest et al. [51] suggested that lithium inter-... 

The measurement of TSH was originally based on bioassays such as the stimulation of colloid droplet formation in the guinea pig thyroid gland and the release of labeled thyroidal iodide into mouse blood. These early in vivo bioassays, however, were of limited sensitivity and precision and were not applicable to the measurement of TSH in unfractionated serum. Most TSH bioassays have involved the in vitro stimulation of thyroid cyclic adenosine monophosphate (cAMP) or adenylate cyclase activity. The rat FRTL-5 thyroid cell line is an example of a particularly convenient and precise assay system. Unfortunately, such methods require purification and concentration of TSH from serum before assay. Sensitive detection of TSH in unfractionated serum is possible using a cytochemical bioassay, but this procedure is technically difficult and time-consuming. At present, immunoassay is the procedure of choice for the measurement of serum TSH in the clinical laboratory. 

Cyclic adenosine monophosphate (cAMP) activates PKA, which in turn phosphor-ylates Cx43 in rat cardiomyocytes.33 Increases in the cAMP concentration increase electrical conductance between paired cardiomyocytes31,34,35 and increase cell permeability - assessed as dye transfer - in non-cardiomyocytes.36 38 Apart from increased cell-cell conductance and permeability, cAMP also increases the extent of gap junction formation.36 38 Increased cAMP concentration results from its enhanced production following stimulation of adenyl cyclase or from inhibition of phosphodiesterase III secondary to an increased concentration of cyclic guanosine monophosphate (cGMP).39-41... 

Trager, W., and Gill, G. S. (1989). Plasmodium falciparum gametocyte formation in vitro Its stimulation by phorbol diesters and by 8-bromo cyclic adenosine monophosphate. ]. Protozool. 36,451-454. 

Features of lithium-induced hyperparathyroidism include a) a low urinary calcium excretion and the absence of nephrolithiasis b) normal urinary cyclic adenosine monophosphate excretion and c) normal plasma inorganic phosphate [30]. In lithium-induced hypercalcemia, a higher frequency of conduction defects has been noted [42]. Lithium also inhibits parathyroid hormone-mediated renal reabsorption of Ca and Mg and blunts parathyroid hormone-mediated phos-phaturia [43]. Lithium interferes with the formation of renal cyclic adenosine monophosphate, which is regulated by parathyroid hormone. Levels of minary cy-... 

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