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 distribution and classification of histamine receptors in mammalian and avian tissues have been summarized in Tables 1-4. It is evident that histamine receptors are present on a number of morphologically distinct cell types and the proportion of cells bearing H1- and H2-receptors varies not only with the species but also with the cell source. The pharmacological receptors mediating mepyramine-sensitive histamine responses have been defined as H1-receptors. Receptors mediating mepyramine-resistant, but burimamide or metiamide-sensitive histamine responses have been classified as H2-receptors. Histamine responses mediated via H2-receptors seem to involve the adenylcyclase system resulting in elevation of intracellular cyclic-AMP level, which is susceptible to burimamide blockade but insensitive to beta-adrenergic blocking agents. This mode of action of histamine involving H2-receptors and the adenyl cyclase system has been shown to stimulate the mammalian heart; promote gastric acid secretion; inhibit antigen-induced histamine release from leucocytes and inhibit lymphocyte-mediated cytotoxicity. It can further be concluded that both H1- and H2-receptors are widely distributed throughout the animal body in the gastro-intestinal, reproductive, respiratory and cardiovascular systems, nervous system and on mast cells and blood leucocytes. In these tissues, histamine receptors play an important role in physiological, immunological and immunopathological processes. Interaction of histamine with both H1- and H2-receptors in varying proportions modulates the overall manifestation of cardiovascular and respiratory syndromes during certain immunopathological conditions (e.g. inflammation, allergy and anaphylaxis). Histamine receptors also appear to play and important role in the development of immuno-competence and immunity.
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PMID:Classification and biological distribution of histamine receptor sub-types. 0 79

Histamine activated adenylate cyclase in pig skin (epidermal) slices, resulting in the accumulation of cyclic AMP. This effect was highly potentiated by the addition of cyclic AMP-phosphodiesterase inhibitors (theophylline, papaverine). A specific H2 receptor inhibitor (metiamide) inhibited the effect of histamine completely, while other antihistamines (diphenhydramine, acetophenazine, perphenazine, fluphenazine, promethazine) inhibited the effect of histamine to various lesser degrees. It has been shown that both epinephrine and prostaglandin E stimulate epidermal adenylate cyclase. Our data using specific blocking agents indicate that histamine, epinephrine and prostaglandin E2 act independently on the epidermal adenylate cyclase system.
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PMID:Histamine (H2) receptor-adenylate cyclase system in pig skin (epidermis). 0 11

Electrophysiological and mechanical effects of histamine were observed in guinea-pig papillary muscle which had been depolarized and rendered inexcitable by elevation of potassium concentration in Tyrode solution to 27 mM. 1. Histamine (3 X 10(-7) to 3 X 10(-5) M) restored the action potential and tension development. The amplitude of the action potential was increased by 31.6 mV/10-fold increase in extracellular Ca2+ concentration. Nifedipine (10(-6) M) abolished the electrical and mechanical responses which had been restored by histamine (10(-5) M) but TTX (10(-5) M) did not affect them. Reduction of the extracellular Na+ concentration to one half decreased the amplitude and the maximum rate of rise of the action potential restored by histamine (10(-5) M) while the peak tension was increased and an after-contraction occurred. 2. The maximum rate of rise and the amplitude of the action potential restored by histamine (10(-5) M) decreased with increase in stimulus frequency from 0.1-1.6 Hz. The peak tension decreased and then increased. The shape of the developed tension was also changed. In the presence of caffeine (1 mM), the only effect of an increase in stimulus frequency was a decrease in peak tension but the change in the shape of developed tension did not occur. 3. The electrical and mechanical responses restored by histamine (3 X 10(-6) or 10(-5) M) were depressed by metiamide (3 X 10(-6) M) but not by diphenhydramine (10(-5) M) or bufetolol (10(-6) M). 4. The electrical response restored by histamine (10(-6) or 10(-5) M) was enhanced by papaverine (10(-5) M) and depressed by N-methylimidazole (10 mM). It is concluded that histamine may enhance the slow inward Ca2+ current mediated by histamine H2-receptors and the adenylate cyclase system in ventricular muscle and that the positive inotropic action of histamine may be attributed to these mechanisms.
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PMID:Restoration by histamine of the calcium-dependent electrical and mechanical response in the guinea-pig papillary muscle partially depolarized by potassium. 1 80

Histamine stimulates adenylate cyclase activity in a washed membrane preparation from guinea-pig ventricle. Marked synergistic effects are observed with histamine and GTP. In the absence of GTP, the degree of stimulation of the enzyme by histamine is slight and occurs only in the presence of relatively high concentrations of ATP suggesting that ATP, or contaminating GTP in commercial preparations of ATP, may partially satisfy the guanylnucleotide requirement. The GTP analog, GppNHp, strongly and irreversibly activates the cardiac enzyme. Preincubation studies, in which the membranes are treated with GppNHp alone or in combination with histamine followed by estensive washing, indicate that histamine markedly increases the rate of activation of the enzyme by the guanylnucleotide. It is suggested that the mechanism of action of histamine on adenylate cyclase involves a facilitation of the interaction of guanylnucleotides with the regulatory site of the enzyme. The relative activities for stimulation of adenylate cyclase of a series of histamine analogs correlate quite well with the activities of these derivatives on four H2-receptor systems, including atrial rate and ventricular contractility and do not correlate with the activities on H1-receptors. The H2-receptor antagonists, burimamide and metiamide, competitively inhibit hitamine-stimulated adenylate cyclase and the dissociation constants for these antagonists on the enzyme agree with the pharmacological data on the H2-receptors in the atria and ventricles. Our results suggest that histamine-stimulated cardiac adenylate cyclase can be classified inotorpic and chronotropic effects of histamine on the intact heart.
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PMID:The interaction of histamine and guanylnucleotides with cardiac adenylate cyclase and its relationship to cardiac contractility. 1 98

1. Dibutyryl cyclic AMP (Db cAMP, 75-500 microgram/kg), injected into the lateral ventricle of the brain of the cat increased blood pressure, heart rate and splanchnic discharge rate. 2. ATP, but not AMP, induced similar changes; GMP in small doses increased blood pressure. 3. A number of drugs are known to activate adenylate cyclase-induced hypertension, tachycardia and increase splanchnic discharge rate. This was shown for TRH, tetracosactide and a new beta2-adrenoceptor stimulant, NAB 365. 4. Injection into the lateral ventricle of theophylline or Ro 7/2956, both inhibitors of phosphodiesterase, similarly increased blood pressure. 5. Histamine administered by the same route induced similar reactions; it is not known if this action was exerted by activation of H1- or H2-receptors. 6. Somatostatin, known to reduce cAMP levels, induced a small but significant decrease in blood pressure. Melanocyte stimulating hormone release inhibiting factor (MIF) and TSH were ineffective. 7. These results provide evidence for the possibility of a role for cAMP in the central regulation of blood pressure at suprabulbar levels.
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PMID:Cyclic 3'5'-adenosine monophosphate and central circulatory control in cats and dogs. 2 Feb 56

Based on the current experimental evidence, a model is proposed for mutual interactions of histamine, prostaglandins, and cyclic AMP in regulation of gastric secretion and pathogenesis of peptic ulcer. Histamine acting on H2-receptor-associated adenylate cyclase stimulates cyclic AMP formation and consequently secretion of hydrochloric acid in oxyntic cells. Prostaglandins (mainly E type) in another cell population stimulate cyclic AMP formation which may lead to formation of glycosaminoglycans and glycoproteins. Glycosaminoglycans and glycoproteins may have antisecretory and cytoprotective properties. In addition to this effect, prostaglandin endoperoxides may inhibit histamine-stimulated cyclic AMP formation in oxyntic cells.
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PMID:Interrelationships between histamine, prostaglandins, and cyclic AMP in gastric secretion: a hypothesis. 2 Mar 85

The response of the cyclic nucleotide system (cAMP, cGMP, adenylate cyclase, guanylate cyclase, and specific phosphodiesterases) to two gastric acid secretagogues, histamine and acetylcholine, and two secretory inhibitors, prostaglandin E2 and secretin, was studied in vivo and in vitro in canine gastric fundic mucosa. Histamine and acetylcholine in vivo failed to stimulate cAMP but significantly increased cGMP; in vitro they affected neither adenylate cyclase nor guanylate cyclase. Prostaglandin E2 and secretin, however, increased cAMP in vivo and significantly stimulated adenylate cyclase in vitro. Specific phosphodiesterases were unaffected by these compounds. The changes, while not specifically localized to the acid-producing cells, are consistent with the suggestion that the control of canine gastric acid secretion may be mediated by changes in mucosal cAMP and cGMP.
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PMID:Cyclic nucleotides and the regulation of canine gastric acid secretion. 3 56

The influence of oxyfedrine on the cardiostimulatory effects of aminophylline was studied in the isolated perfused guinea-pig heart. It was found that oxyfedrine potentiated the stimulatory effects of aminophylline on isometric contraction, dF/dt, coronary flow and heart rate. This potentation was abolished after pretreatment with propranolol. Histamine, though to a lesser extent, also potentiated the effects of aminophylline. When oxyfedrine and histamine were infused simultaneously in the presence of propranolol, the response of the heart to aminophylline was also potentiated; the magnitude of this potentiation was comparable to that obtained with histamine alone, indicating that propranolol abolished only the action of oxyfedrine but not that of histamine. The mechanical effects of aminophylline were accompanied by a slight (15 per cent) but significant inhibition of phosphodiesterase, which was not further augmented by oxyfedrine. The results suggest that the potentiating effects of oxyfedrine or histamine on the cardiostimulatory actions of aminophylline are elicited by their stimulatory actions on adenylate cyclase activity.
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PMID:Potentation of the cardiac response to aminophylline by oxyfedrine. 16 89

Adrenal cAMP and plasma corticosterone levels were determined in pre-weanling rats subjected to treatment with either ACTH (50 mU/rat) or histamine dihydrochloride (0.2 mg/g body wt). ACTH injection elevated both serum corticosterone and adrenal cAMP levels on all days tested. However, the ACTH-induced elevation of adrenal cAMP and serum corticosterone both diminished steadily from day 2 to day 8 and then increased from day 8 to day 16. Histamine injection resulted in elevated serum corticosterone levels in a pattern similar to that of the corticosterone response to ACTH. However, histamine injection did not result in any significant increase in adrenal cAMP from day 2 to day 10. From day 12 to day 16 the adrenal cAMP concentration rose steadily in parallel with ther serum corticosterone levels. These results indicate: (1) that a functional, ACTH-sensitive adenyl cyclase system is present in the adrenal gland of the immature rat, (2) that the responsiveness of this system diminishes during the first postnatal week before returning to its previous 2-day-old capacity by day 16, and (3) that during the first few days after birth, histamine stress results in elevated serum corticosterone levels without elevating adrenal cAMP levels.
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PMID:Effect of ACTH and histamine stress on serum corticosterone and adrenal cyclic AMP levels in immature rats. 16 40

The regulation patterns of gastric acid secretion in rats were investigated. Pentagastrin and histamine stimulate gastric acid secretion, but the inhibitors of DNA-dependent synthesis of RNA and of proteins prevent only the pentagastrin action. It has been found that pentagastrin induces histidine decarboxylase in gastric mucosa, ensuring local accumulation of histamine. The latter activates adenylate cyclase and results in 3',5'-AMP accumulation in gastric tissues. The administration of pentagastrin, histamine or 3',5'-AMP enhances the activity of gastric carbonic anhydrase, the enzyme which takes part in HCl formation. The data suggest that these three compounds act sequentially (pentagastrin leads to histamine leads to3',5'-AMP) and the effect of the last one could be mediated through 3',5'-AMP dependent protein kinase. The experiments in vitro demonstrated that gastric carbonic anhydrase can be separated into two isoenzymes and thephosphorylation of one of them by the 3',5'-AMP dependent protein kinase sharply increases its activity. The findings raise the possibility that histamine and 3',5'-AMP, mediating gastrin action, form together with enzymes (histidine decarboxylase, adenylate cyclase, protein kinase, carbonic anhydrase) a caascade of amplifiers. Autoradiographic studies have shown that [3H]-pentagastrin is not bound by oxyntic cells but adheres preferentially to histamine-producing alpha-like endocrine cells and to the chief cells, while 3H-histamine adheres preferentially to oxyntic and to chief cells. Electron microscopy indicates that only pentagastrin (but not histamine) initiates in alpha-like endocrine cells ultrastructural changes characteristic for induction. Pentagastrin, histamine and 3',5'-AMP administration produces in oxyntic cells ultrastructural changes typical for the secretion processes. These results lead to assumption that pentagastrin (gastrin) induces histidine decarboxylase in alpha-like endocrine cells of gastric glands. Histamine which is secreted enhances adenylate cyclase activity in the neighbouring oxyntic cells where 3',5'-AMP dependent protein kinase activates carbonic anhydrase by means of phosphorylation. These different cells form, probably, a multicellular functional unit for gastric acid secretion.
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PMID:Integration of biochemical functions of different cells of rat gastric mucosa for hydrochloric acid secretion. 18 10


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