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)

Anoxia (during 2 minutes after decapitation) produced a significant elevation of cAMP contents (up to 410%) in mouse brain cells. This effect was abolished by an intraperitoneal injection of alloxan (A), morphine (M), and ethanol (E) 30 minutes before decapitation, and after a 2 minutes diethyl ether (DE) inhalation. It was found that anoxia produced some decrease in phosphodiesterase (FDE) activity. A preliminary injection of A and E produced an activation of FDE; M and DE did not change FDE significantly. Mechanisms of action of all the four agents on the cAMP content under anoxia are different. A and E produced a rapid cAMP hydrolysis on stimulating the activity of FDE, M and DE inhibited apparently adenylate cyclase. The activation of adenylate cyclase due to anoxia is considered as one of the initial steps in the cell injury extention.
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PMID:[Increase in the cAMP content of mouse brain cells in ischemia and inhibition of this effect by certain biologically active compounds]. 626 87

Factors regulating the release of phosphatidylcholine (PC) from neonatal-rat lungs were investigated. The results show that the release of prelabelled PC from the newborn-rat lung was augmented by air ventilation at the onset of breathing. This response was mimicked in lungs of pups delivered 1 day before term and allowed to breathe for different time intervals. Anoxia further augmented the ventilation-enhanced PC release from the newborn-rat lungs. The ventilation-induced release of PC was not abolished by the prior treatment of pups in utero or mothers in vivo with phenoxybenzamine, propranolol or atropine, suggesting the lack of receptor stimulation in the ventilation-enhanced PC release at birth. The results also show that ventilation stimulated [methyl-14C]choline incorporation into lung PC, presumably to replenish the depleted surfactant stores. The ratio of adenylate cyclase/cyclic AMP phosphodiesterase activities, which reflects cyclic AMP levels in the developing rat lungs, did not change during the 120 min of air ventilation when the release of PC was much enhanced, implying that cyclic AMP may not be involved. This confirms our conclusion that stimulation of beta-adrenergic receptor was not involved in the air-ventilation-enhanced release of PC. Since the cell number or size did not change during 120 min of ventilation when the alveolar-cell surface was maximally distended, it is suggested that distension of alveolar wall by air ventilation at the onset of breathing may bring the lamellar bodies containing surfactant close to the luminal surface of alveolar type II cells, thereby enhancing their fusion and extrusion by exocytosis.
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PMID:Ventilation-induced release of phosphatidylcholine from neonatal-rat lungs in vitro. 647 85

Crude myocardial sarcolemmal membrane fractions were prepared from rat hearts subjected to total global ischemia with and without normoxic reperfusion, or global anoxic (N2) perfusion with and without normoxic reperfusion. The direct effects on beta-adrenoceptor number, G-protein levels and stimulation of the adenylate cyclase (AC) complex were assessed. In terms of AC activation, ischemia led to a marked increase (4-fold) in sensitivity to terbutaline (beta2-agonist) and phorbol ester (tetradecanoyl phorbol acetate = TPA) stimulation, whereas the dobutamine (beta1) responsiveness and Gpp(NH)p activation through G(s)alpha/G(i2)alpha remained unaltered. However, forskolin-elicited holoenzyme activity fell markedly during normoxic reperfusion. Ischemia did not change the beta1-adrenoceptor number, while beta2-receptor population increased by approximately 45%. Western blots of myocardial G(s)A and G(i2)alpha contents revealed that ischemia selectively diminished G(i2)alpha levels only by some 50-70%. Contrastingly, anoxia selectively increased the AC sensitivity (2-fold) to beta1-adrenergic stimulation. As subsequent to ischemia, anoxia also increased the sensitivity to TPA stimulation, however, only 2-fold. Gpp(NH)p activation was unchanged, while forskolin-enhanced activity gradually declined, also during ensuing normoxic reperfusion. Anoxia brought about a 75% enhancement in beta1-receptor number, while beta2-receptors remained unaffected. However, altered receptor number normalized on termination of normoxic reperfusion. Finally, anoxia led to a 50-60% decimation of myocardial G(i2)alpha levels, while G(s)alpha was only marginally reduced. Despite the fact that the ischemia and anoxia effectuated a similar deterioration of physiological heart parameters, myocardial contents of energy rich phosphate moieties and loss of G(i2)alpha, ischemia rendered the most profound increase in responsiveness of the sarcolemmal AC system.
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PMID:Enhanced responsiveness of the myocardial beta-adrenoceptor-adenylate cyclase system in the perfused rat heart (I). 1019 81

The distribution of cyclic GMP, cyclic AMP and related enzymes in the vertebrate retina, together with factors regulating their levels, are described. Photo-receptor cells in retinas from all species examined contain very high levels of cyclic GMP and high activities of both guanylate cyclase and cyclic GMP phosphodiesterase. In more proximal regions of the retina, cyclic GMP is found at concentrations similar to that of brain. Guanylate kinase and GDP kinase, enzymes involved in GMP metabolism, also have increased activities in photoreceptor cell layers although their pattern of distribution does not exactly parallel that of cyclic GMP. The concentration of cyclic AMP is fairly uniform throughout the retina and at a level similar to that found in other areas of the CNS. However adenylate cyclase has an uneven distribution with particularly high activity in the inner plexiform layer. Cyclic nucleotide levels in retina may be modified by several factors. Light decreases both cyclic nucleotides in rod-dominant retinas, although we have not observed similar changes in cone-dominant retinas. Anoxia or ischemia elevates cyclic AMP and decreases cyclic GMP, similar to other areas of CNS, while incubation of retina in Ca(++)- free media markedly increases cyclic GMP levels, an effect opposite that seen in brain tissue. Depolarization of retina with high K(+) causes a modest elevation of cyclic AMP but has no effect on cyclic GMP, which is also significantly different from the response in brain. Cyclic AMP levels in retina however, can be elevated by dopamine which is an effect similar to that in striatum. These data indicate that there are probably multiple cyclic GMP and cyclic AMP systems in retina, some of which may be unique to this tissue.
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PMID:Localization and roles of cyclic nucleotide systems in retina. 2048 44