Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:4.6.1.1 (adenylate cyclase)
19,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of the boiled supernatant on synaptosomal adenyl cyclase activity of rat cerebral cortex was investigated. The boiled supernatant markedly increased the accumulation of cyclic AMP in synaptosomes when added to adenyl cyclase system by a mechanism presumably unrelated to inhibition of cyclic AMP phosphod iesterase or adenosine triphosphatase. Magnesium ion was required for synaptosomal adenyl cyclase activity and its stimulation by the boiled supernatant. The result discerned by doubl reciprocal plots showed an increase in Vmax value of adenyl cyclase by addition of the boiled supernatant without significantly altering the affinity for substrate. The enzyme activity was not stimulated by dopamine, histamine and serotonin in either the absence and presence of the boiled supernatant.
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PMID:The stimulatory effect of the boiled supernatant on cyclic AMP formation in synaptosomes from rat cerebral cortex. 17 9

Estrogen induces blastocyst implantation in diapausing female mice, increases uterine levels of adenyl cyclase and cyclic adenosine monphosphate (cylic AMP), and stimulates synthesis of ribonucleic acid and protein in both the uterus and blastocyst. Furthermore, the surface ultrastructure of trophoblast cells seen with scanning electron microscopy (SEM) changes with activation of the diapausing blastocyst by estrogen. Cyclic AMP-activated blastocysts were investigated with the use of SEM and compared to blastocysts activated by estrogen. Intraperitoneal administration of cyclic AMP was generally ineffective, whereas administration of cyclic AMP intraluminally in the uterus effectively mimicked the early estrogen activation. These findings are discussed in relation to other known activation changes in preimplantation blastocysts and with regard to similar findings after administration of various antiestrogens.
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PMID:Cyclic adenosine monophosphate-induced changes in the surface morphology of diapausing blastocysts and the effects on implantation. 17 29

The present study was undertaken to evaluate the effects of methoxamine on force development and adenyl cyclase activity in cat ventricular myocardium. Methoxamine produced a dose-related increase in force development of isometrically contracting cat papillary muscles. The positive inotropic effects of methoxamine were not altered by beta-adrenergic blockade (propranolol), or catecholamine depletion by prior reserpinization, but were completely prevented by alpha-adrenergic blockade (phentolamine or ergotamine). Neither ergotamine, phentolamine, nor methoxamine had any direct effects on adenyl cyclase activity. Phentolamine did not attenuate the increase in force development produced by paired electrical stimulation, suggesting that it does not block the entry of calcium into the muscle. In summary, methoxamine produced a dose-related increase in force development of the cat papillary muscle that was selectively blocked by alpha-adrenergic receptors in ventricular myocardium.
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PMID:Positive inotropic effects of methoxamine: evidence for alpha-adrenergic receptors in ventricular myocardium. 17 42

The 24-hour urinary excretion of cyclic 3',5'-adenosine monophosphate (cAMP) was measured by a protein-binding assay in 55 healthy volunteers (aged 20-35 yr) and in 30 hospitalized elderly subjects (aged 70-93 yr). In the older subjects the mean 24-hour cAMP excretion was significantly lower; the correlation between cAMP excretion and age demonstrated a progressive decrease from the age of 70 to the tenth decade. Many different factors could account for the reduced urinary cAMP excretion in elderly subjects: a decline in the reactivity of the adenyl cyclase-cAMP system related to physiological ageing; reduced physical activity; a reduction in the glomerular filtration rate or decreased production of cAMP by tubular cells in the senile kidney.
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PMID:Urinary cyclic adenosine monophosphate in young adults and elderly subjects. 17

Prostaglandin E was found to increase the formation of cyclic acdenosine 3',5'-monophosphate (cyclic AMP) by renal cortical slices. This increased release of cyclic AMP was not influenced by the absence of Ca2+ in the incubating media. The enhanced production of cyclic AMP was probably mediated by stimulation of membrane-bound adenylate cyclase activity. An increase in adenyl cyclase activity was observed with increasing concentrations of prostaglandin E. Furthermore, prostaglandin E augmented glucose production from alpha-ketoglutarate. This effect on gluconeogenesis was abolished by the removal of Ca2+ from the incubating medium. These effects are similar to those described for parathyroid hormone and suggest that the renal cortex is a prostaglandin-dependent system. Prostaglandin E decreased cyclic AMP production and glucose production (from alpha-ketoglutarate) in response to submaximal doses of parathyroid hormone, suggesting that prostaglandin may be important in modulating the intracelluar action of parathyroid hormone in the kidney cortex.
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PMID:Effect of prostaglandin E on the adenyl cyclase-cyclic AMP system and gluconeogenesis in rat renal cortical slices. 17 40

Cholera enterotoxin, 45 mug per 250 g body weight, administered intravenously to rats, caused a 6-fold rise in the activity of liver alkaline phosphatase in 12 hr. There was no change in bile volume or in the concentration or total bile content of Na+, K+, HCO3-, or Cl- for 36 hr after the administration of cholera toxin. However, bile phospholipid output fell markedly from a control level of 15.0 +/- 1.0 mumol per 6 hr to a low level of 4.0 +/- 1.2 mumol per 6 hr in the 12- to 18-hr collection, P less than 0.001. There was a similar fall in bile acid secretion, from a control value of 9.8 +/- 0.4 mumol per 6 hr to 4.1 +/- 0.9 mumol in the 12- to 18-hr period, P less than 0.01. The cholera effect was prolonged. Bile acid and phospholipid secretion rates did not return to control values until 30 to 36 hr after the administration of cholera enterotoxin. The cholera toxin-induced reductions in bile acid and phospholipid secretion into bile did not appear to be mediated by adenyl cyclase or cyclic AMP because neither glucagon, a known stimulator of liver adenyl cyclase, nor dibutyryl cyclic AMP had any effect on the secretion into bile of bile acids or phospholipid. The administration of cholera toxin was not associated with any increase in the secretion of free choline into bile. Glucagon and dibutyryl cyclic AMP, two other substances known to increase the activity of rat liver alkaline phosphatase, also had no stimulatory effect on the secretion of free choline into bile. The results do not support the hypothesis that the main function of rat liver alkaline phosphatase is to facilitate the excretion of free choline into bile.
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PMID:Effects of cholera enterotoxin, glucagon, and dibutyryl cyclic AMP on rat liver alkaline phosphatase, bile flow, and bile composition. 17 82

The energy charge potential of the cerebral adenylate system, the cerebral lactate: pyruvate system, and the cerebral glycogen level were used to characterize the cerebral energy state of the brain. Cerebral adenyl cyclase activity and cyclic AMP concentrations were investigated to evaluate their possible influence on the regulatory processes in brain metabolism. These biochemical parameters were evaluated on the cortical motor area of the brain of the beagle dog in hypovolaemic hypotension during acute hypoxia (obtained by altering the composition of the inhalation mixture) and during the post-hypoxic recovery (three minutes after the restoration of normal ventilation). This experimental model of acute hypoxia was also used for investigating the action of some substances acting at beta-adrenergic receptor level or at vascular level. The substances were perfused into the carotid artery at the rate of 0.5 ml/min for three to six minutes. During the first stage of hypoxia, the adenyl cyclase system is probably an important biochemical regulatory factor. This system becomes less important when a critical threshold is crossed (oxygen arterial partial pressure less than 25-20 mmHg) below which other factors become rate-limiting. A beta-receptor stimulating agent enhanced the mechanisms of physiological post-hypoxic recovery; inhibition of this action was obtained with a beta-receptor blocking agent. Under these experimental conditions, no correlation existed between the vascular effects of the agents and brain metabolism.
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PMID:Adenyl cyclase system and cerebral energy state. 17 28

In the first part of this paper, a short review of the literature on the effects of catecholamines, Ca2+, and cyclic AMP on the biochemical, electrical, and mechanical properties of the heart is presented. It is concluded that the effects of epinephrine on activation of glycogenolysis and on the inotropic response of cardiac muscle are both mediated by the combined actions of Ca2+ and cyclic AMP. Since the inotropic response precedes the glycogenolytic response it is evident that increased energy metabolism is a consequence of increased heart work and not a causative factor. The available data suggest that increased tissue cyclic AMP levels resulting from catecholamine stimulation of adenyl cyclase activity alter cardiac mechanics by modulation of the basic calcium flux cycle of the heart. These effects may be mediated by cyclic AMP-stimulated phosphorylation of specific proteins located in the sarcolemma, sarcoplasmic reticulum, and myofilaments via one or more protein kinases, although experimental verfication of the possible relationship between protein phosphorylation and altered Ca2+ binding properties at specific sites in the membranes is at present largely lacking. The increased rate of tension development induced by catecholamines appears to be caused by an increased rate of Ca2+ influx across the sarcolemma during the plateau phase of the action potential, whereas the increased rate of relaxation is probably attributable to an increased rate of sequestration of intracellular Ca2+ by the sarcoplasmic reticulum. In the second part of the paper, data are presented using a working rat heart preparation to illustrate the effect of catecholamines in facilitating Ca2+ entry across the sarcolemma. Decreased left ventricular pressure development induced by addition of ruthenium red or verapamil to inhibit Ca2+ influx was relieved in a concentration-dependent manner by catecholamines. Curves of percentage change of left ventricular pressure against external Ca2+ concentration are presented which show that epinephrine increased the sensitivity of the heart to Ca2+ whereas verapamil decreased it. A half-maximal increase of left ventricular pressure was obtained with 0.6 mM Ca2+ in control hearts, 0.3 mM Ca2+ with epinephrine, and 2.9 mM Ca2+ with verapamil (10(-7)-treated hearts. Verapamil combined with epinephrine at the above concentrations gave a half-miximal increase of left ventricular pressure with 1.3 mM Ca2+. These results are discussed in relation to a model for the Ca2+ flux in the heart.
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PMID:Epinephrine, cyclic AMP, calcium, and myocardial contractility. 17 96

Clearance studies were made to determine the influence of intravenous infusions of dopamine (between 2.5 and 3.5 mug.kg.-1min.-1) on renal function and on the adenyl cyclase phosphodiesterase system in eleven patients with chronic renal disease. Glomerular filtration rate (+ 19%), effective renal plasma flow )+ 29%), sodium (+ 199%) and potassium (+ 40%) clearances were significantly increased. These effects were associated with a stimulation of the adenyl cyclase phosphodiesterase system demonstrated by an increase of cyclic adenosine 3'5'-monophosphate in plasma and urine. The results suggest that dopamine probably affects renal function by activating the adenyl cyclase phosphodiesterase system.
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PMID:Effects of dopamine on kidney function and on the adenyl cyclase phosphodiesterase system in man. 17 93

[3H]-Catecholamine binding to intact cells, isolated cell membranes, and to several isolated macromolecules has been shown by several laboratories to be neither stereospecific nor inhibited by known beta-antagonists. Since additional evidence indicates that this binding is not an artifact (i.e. due neither to the binding of a catecholamine oxidation product nor hormone binding to a catabolic enzyme such as COMT), the question remains as to whether this represents binding to a bona fide membrane receptor. Because all ligands which bind strongly or compete for this binding possess a catechol group, one possible explanation is that the binding affinity is primarily determined by the catechol moiety, whereas the correct stereoisomer of the side chain is necessary to activate the receptor. Thus, although binding is a necessary condition for hormone action, the necessary and sufficient condition for activation of adenyl cyclase is both the catechol group and the correct stereoisomer of the side chain. A theoretical model is developed here to provide a quantitative basis for this hypothesis. This model extends the current concept of distinct subunits in the adenyl cyclase system by separating the receptors from the catalytic sites and placing them at separate locations within the membrane. Utilizing the spare receptor model of Furchgott, and the mobility of macromolecules within a "lipid sea," the appropriate equations to predict both hormone binding and enzyme activation are derived. Using the observed affinity constants from catecholamine binding studies, it is then shown that this model can predict the experimental observation and hence explain the apparent dichotomy arising from binding enzyme activation studies.
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PMID:Hormone receptor mobility and catecholamine binding in membranes. A theoretical model. 17 17


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