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PubMed1978

Role of cyclic AMP in rat aortic microsomal phosphorylation and calcium uptake.

The role of adenosine 3',5'-monophosphate (cyclic AMP)-dependent membrane phosphorylation in the regulation of microsomal calcium transport in rat aortic smooth muscle was studied. Cyclic AMP-dependent protein kinase augmented the phosphorylation of serine residues in a microsomal protein component with a molecular weight of about 44,000 (determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis) and the majority of 32P incorporation was in serine residue(s). The phosphorylated protein had stability characteristics of a phosphoester. The phosphorylated substrate was not extracted from the trichloroacetic acid (TCA) precipitate with organic solvents or by suspension in hot TCA; and the demonstrated hydroxylamine insensitivity suggested that the substrate was not lipid or nucleic acid. Intrinsic phosphoprotein phosphatase cleaved the labeled phosphate from the cyclic AMP-stimulated microsomes in the first 5 min of incubation. Microsomes phosphorylated in the presence of 1 micron cyclic AMP or 1 micron cyclic AMP plus 0.1 mg/ml protein kinase exhibited enhanced calcium uptake. We suggest that reversible phosphorylation of microsomal membranes may play an important role in the regulation of aortic microsomal calcium transport by cyclic AMP.

Animals↗
PubMed1985

Beta-adrenergic stimulation of adenosine-3',5'-monophosphate (c-AMP) in primary cultures of rat anterior pituitary cell populations separated by unit gravity sedimentation. Relationship to growth hormone and prolactin release and to nonsecreting cells.

The effect of the beta-adrenergic agonist isoproterenol (ISO) on c-AMP accumulation and on growth hormone (GH) and prolactin (PRL) release was studied in primary cultures of anterior pituitary cell populations with different proportional number of somatotrophs and lactotrophs, obtained by velocity sedimentation at unit gravity. ISO stimulated c-AMP levels in highly-enriched lactotroph (approximately 70%) as well as in highly-enriched somatotroph (approximately 65%) populations. ISO-stimulated c-AMP accumulation was attenuated by dopamine (DA) in highly enriched lactotroph but not somatotroph populations. In a small-cell population consisting of a much lower proportional number of lactotrophs and somatotrophs, the proportional increase of c-AMP accumulation was several times higher than in the other populations and the effect was not suppressible by DA. In this small-cell population, GH but not PRL release was more responsive to ISO than in the other populations. The present observations are consistent with the interpretation that the changes in c-AMP levels induced by ISO originate in part in somatotrophs and lactotrophs. However, the present data also demonstrate that the most responsive cell population in terms of c-AMP accumulation consists of small cells. The majority of these cells could not be identified. The possibility that these cells may be nonsecreting folliculostellate cells is discussed.

Animals↗
PubMed1979

Dissociation between cardiac cyclic AMP and myocardial contractility induced by verapamil, calcium and magnesium ions.

Isolated, perfused rat hearts were used to study the effects of verapamil, excess calcium ions or excess magnesium ions on changes in heart cyclic AMP and myocardial force of contraction. Verapamil caused a dose-dependent decrease in force of contraction and a nondose-related reduction in cyclic AMP. Perfusion of hearts with medium containing 5 mM calcium produced a significant rise in cyclic AMP, but no change in contractile force. The depressant effects of verapamil on contractility and cyclic AMP were reversed by 5mM calcium; excess calcium in the perfusion fluid also containing verapamil prevented the myocardial depressant effects of verapamil. Acutely elevating the magnesium concentration in the perfusion medium decreased force of contraction, accentuated the negative inotropic effect of verapamil, but did not decrease cyclic AMP or enhance the verapamil-induced reduction in cyclic AMP.

Animals↗
PubMed1992

Effects of dobutamine and terbutaline on adenylate cyclase activity and cyclic AMP content in the renal pelvis of rabbits.

We measured the adenylate cyclase activity and the cyclic AMP content of the upper and lower renal pelvis in rabbits in order to clarify whether cyclic AMP acted as the intracellular messenger of the response elicited by beta-agonists in renal pelvic smooth muscle. Adenylate cyclase activity was determined by the method of Salomon et al. and tissue cyclic AMP content by radioimmunoassay. Dobutamine elevated the adenylate cyclase activities and tissue cyclic AMP contents of the upper part of the renal pelvis more than those of the lower part of the renal pelvis. Terbutaline also elevated the adenylate cyclase activities and tissue cyclic AMP contents of both the upper and lower part of the renal pelvis. The terbutaline-induced increase was the same in the upper and lower pelvis. These data suggest that cyclic AMP acts as the intracellular second messenger in renal pelvic smooth muscle of rabbits. Furthermore it is thought that both beta 1- and beta 2-adrenergic receptors exist in rabbit renal pelvis and the distribution of these beta-receptor subtypes is different between the upper and lower part of the renal pelvis.

Adenylyl Cyclases↗
PubMed1984

Prostaglandins and intracellular cyclic AMP in respiratory secretory cells.

Prostaglandins are known to affect ion transport and mucus secretion in the trachea, and at least part of their effect is thought to be mediated by cyclic AMP. Because no prostaglandin receptor assay is currently available, we have used an immunocytochemical probe for the intracellular localization of cyclic AMP to identify those specific cell types in dog and cat trachea that respond to prostaglandins. Using tracheal explants similar to those used by other investigators for in vitro studies of ion transport and glycoprotein secretion, we examined the effect of endogenous and exogenous prostaglandins on immunoreactive cyclic AMP. Endogenous prostaglandins, which may be secreted in response to minor distortion of tissue membranes, stimulated immunoreactive cyclic AMP in ciliated epithelial cells and in both serous and mucous submucosal gland cells. This was not observed in tissues assayed 60 min after dissection, or dissected in the presence of indomethacin or of BW755C. Exogenous prostaglandin E1 increased cyclic AMP in these same cell types. We conclude that prostaglandins stimulate cyclic AMP in specific cell types in the trachea, and that endogenous prostaglandins play a major role in many in vitro preparations.

Animals↗
PubMed1973

Comparative effects of angiotensin and ACTH on cyclic AMP and steroidogenesis in isolated bovine adrenal cells.

The comparative effects of angiotensin II and adrenocorticotropic hormone (ACTH) on cyclic AMP and steroidogenesis were investigated employing isolated bovine adrenal cells from the zona fasciculata. Like ACTH, angiotensin produced a prompt increase in cyclic AMP which preceded the increase in corticosteroid production. Although this increase in cyclic AMP was small when compared to that induced by ACTH, it correlated with the amount of steroidogenesis. This observation is consistent with the view that cyclic AMP is the intracellular mediator of the steroidogenic action of angiotensin. Angiotensin acted synergistically with ACTH on cyclic AMP levels. This synergism was not explained by inhibition of phosphodiesterase activity. Unlike ACTH, angiotensin failed to stimulate adenylate cyclase in broken cell preparations. The observations suggest that more than one mechanism may be involved in effects of ACTH and angiotensin on cyclic AMP levels.

Adrenal Cortex Hormones↗
PubMed1978

Interaction of polymorphonuclear neutrophils with Escherichia coli. Effect of enterotoxin on phagocytosis, killing, chemotaxis, and cyclic AMP.

Enterotoxigenic Escherichia coli are associated with noninflammatory diarrhea and stimulate adenylate cyclase activity of mammalian cells, thereby increasing intracellular cyclic adenosine 3',5'-monophosphate (cyclic AMP). Increased concentrations of cyclic AMP in polymorphonuclear neutrophils (PMN) inhibit phagocytosis, candidacidal activity, granule discharge, and chemotactic responsiveness. We examined the effect of enterotoxin on the interaction of human PMN with E. coli. Enterotoxigenic and nonenterotoxigenic strains, including serotypes of E. coli identical except for the presence or absence of the plasmid coding for enterotoxin production, were utilized. Enterotoxigenic and nonenterotoxigenic E. coli, tumbled with PMN, were phagocytized and killed (>97%) equally well, and these strains stimulated PMN hexose monophosphate shunt activity equivalently.However, a chemotaxis assay under agarose demonstrated that filtrates of 10 enterotoxigenic strains were less chemotactic for PMN by 15+/-2% total migration or 46+/-1% directed migration, when compared with 6 non-enterotoxigenic strains (P < 0.001). Inactivation of the enterotoxin by heat (65 degrees C for 30 min) or antibodies formed to E. coli enterotoxin eliminated the inhibitory effect of the enterotoxic filtrates for PMN chemotaxis. Addition of purified E. coli enterotoxin directly to the PMN decreased chemotaxis to E. coli filtrates by 32+/-2% (P < 0.001). These data suggest that the effect was due to the heat-labile enterotoxin. The phosphodiesterase inhibitor, 1-methyl-3-isobutylxanthine (0.1 mM), which potentiates effects due to an increase in intracellular cyclic AMP, further decreased total PMN migration (random plus directed) toward enterotoxic filtrates to 46% of that to nonenterotoxic filtrates (P < 0.001). Addition of cholera toxin (1 mug/ml), which is similar to E. coli enterotoxin, to the PMN inhibited total migration toward nonenterotoxic filtrates by 16+/-2% (P < 0.001). Exogenous dibutyryl cyclic AMP (2 mM) inhibited total PMN migration toward E. coli filtrates by 32% (P < 0.001). PMN intracellular cyclic AMP levels increased by 220% after 2 h of incubation with purified E. coli enterotoxin. The decreased chemotactic attractiveness of enterotoxic E. coli filtrates appears to be related to the ability of enterotoxin to increase cyclic AMP in PMN. Enterotoxin production by E. coli may be advantageous to the microbe by decreasing its chemotactic appeal for PMN.

Blood Bactericidal Activity↗
PubMed1995

The effect of cyclic-AMP on the regulation of c-myc expression in T lymphoma cells.

Myc is implicated in the control of growth in a variety of cell types. I investigated c-myc gene expression in several lymphoid cell lines to determine the response to cyclic AMP. Cyclic AMP causes a precipitous decline in c-myc message concentration that precedes G1 cell cycle arrest in wild type S49 cells but not in KIN- cells that lack cAMP dependent PKA activity. In wild-type S49 cells washout of cyclic AMP restores c-myc message levels within 2 h but does not relieve the G1 arrest until 10 h later. Transcription runoff studies demonstrate inhibition of both transcriptional initiation and prolongation of initiated transcripts. However, the degree of inhibition is insufficient to explain the absence of detectable myc message suggesting that the predominant effect of cyclic AMP is to destabilize the c-myc message. In contrast to wild-type cells, the "Deathless" mutant S49 cell line is viable when arrested in G1 by exposure to cyclic AMP and has preserved c-myc expression. Thus, in S49 cells down regulation of c-myc expression appears to be associated with loss of viability rather than G1 cell cycle arrest. Interestingly, CEM human T lymphoma cells do not arrest in G1 phase when exposed to cyclic AMP in spite of losing detectable c-myc gene expression. This suggests that in some T lymphoma cells c-myc gene expression may not be necessary for cell cycle progression and proliferation.

Animals↗
PubMed1979

Influence of aminophylline and cyclic AMP on glycogen metabolism in fetal rat lung in organ culture.

The glycogen content of fetal rat lung declines coincident with increased pulmonary phospholipid synthesis. Aminophylline, a methylxanthine cyclic adenosine 3',5' monophosphate (AMP) phosphodiesterase inhibitor, and cyclic AMP augment fetal lung phospholipid synthesis. Because lung glycogen breakdown may contribute to pulmonary phospholipid synthesis, the effects of aminophylline and cyclic AMP on glycogen metabolism were studied in explants of 19 day fetal rat lung in organ culture. Treatment with aminophylline or dibutyryl cyclic AMP for 24 hr, resulted in a 25% (P less than 0.025) and 75% (P less than 0.001) decrease, respectively, in the glycogen content of the explants. Glycogen synthase I activity was reduced by 32% in aminophylline treated cultures (P less than 0.025) and 25% in cyclic AMP treated cultures (P less than 0.025). The percent of total synthase in the active form was significantly reduced in all treated cultures. Neither aminophylline nor cyclic AMP treatment resulted in significant changes in glycogen phosphorylase a or total phosphorylase activity.

Aminophylline↗
PubMed1975

Effect of porcine calcitonin on the metabolism of calcium and cyclic AMP in rat skeletal tissue in vivo.

Infusion of 50 mU/100 g body wt of calcitonin induced a rapid and marked increase of cyclic AMP in calvaria as well as in plasma of thyroparathyroidectomized rats. These changes preceded the decrease in plasma calcium concentration seen after hormone administration. The possible relationship of this stimulation of cyclic AMP accumulation to the hypocalcemic effect of calcitonin was examined under several experimental settings. It was found that a dose of calcitonin sufficient to cause a significant decrease of plasma calcium failed to produce any detectable accumulation cyclic AMP in calvaria, but when high doses of calcitonin were given, there was an apparent correlation between the integrated change of cyclic AMP metabolism and the duration and magnitude of hypocalcemia. Experiments employing the ophylline and imidazole, which alter cyclic AMP metabolism, led to an apparent dissociation between the hypocalcemic effect of calcitonin and its stimulation of cyclic AMP accumulation in bone.

Animals↗
PubMed1976

Effects of follicle stimulating hormone and luteinizing hormone upon cyclic AMP and cyclic GMP levels in rat ovaries in vitro.

In vitro effects of FSH and LH on adenosine 3',5'-cyclic monophosphate (cyclic AMP) and guanosine 3',5'-cyclic monophosphate (cyclic GMP) levels in rat ovarian tissue were studied. Ovaries from immature rats treated with either pregnant mare's serum (PMS) or PMS and human chorionic gonadotropin (hCG) were incubated at 37 C for 30 min in defined medium 199 containing aminophylline (0.1 mg/ml). Increasing concentrations of LH (0.4-10.0 mug) when added to the medium containing ovaries with predominantly follicular tissue (PMS-treated) produced progressive increases in cyclic AMP (29-300%) and concomitant decreases in cyclic GMP (41-70%). FSH (4-100 mug) added to the medium produced comparable changes in nucleotide levels: cyclic AMP increased 52-390% and cyclic GMP decreased 45-80%. Ovaries with predominantly luteal tissue (PMS- and hCG-treated) responded differently to the same experimental conditions. LH produced a much greater increase in tissue cyclic AMP levels (209-1280%), whereas FSH produced comparable increases in cyclic AMP as seen with follicular tissue (103-570%). Neither gonadotropin caused any changes in cyclic GMP levels in luteinized ovaries. These results indicate that rat ovarian cyclic GMP is regulated by gonadotropins and the differences in the direction of nucleotide response to gonadotropins suggest divergent roles for cyclic AMP and cyclic GMP in ovarian function.

Animals↗
PubMed1998

Regulation of macropinocytosis in v-Src-transformed fibroblasts: cyclic AMP selectively promotes regurgitation of macropinosomes.

Stable transformation of Rat-1 fibroblasts by the v-Src oncoprotein results into the constitutive formation of macropinosomes. In the present report, we found that macropinosomes do not fuse with transferrin-containing endosomes and investigated the effects of cyclic AMP as a regulator of macropinocytosis in this cell system. The permeant analogs dibutyryl cyclic AMP and 8-bromo-cyclic AMP, as well as the pharmacological activator of adenylate cyclase forskolin, similarly decreased by about 35% the net endocytic accumulation of the fluid-phase tracer horseradish peroxidase at intervals >5 minutes in v-Src-transformed cells but not in the non-transformed parental Rat-1 cell line. However, and in contrast to the phospholipase C inhibitor 2-nitro-4-carboxyphenyl-N, N-diphenylcarbamate or the phosphatidylinositol 3-kinase inhibitor wortmannin, dibutyryl cyclic AMP neither returned the peroxidase accumulation rate of v-Src-transformed cells to that of parental Rat-1/control cells, nor prevented macropinosome formation, as shown by confocal microscopy. Detailed analysis of the kinetics of tracer entry and efflux in transformed cells revealed that dibutyryl cyclic AMP inhibited peroxidase accumulation only after intervals >5 minutes, due to accelerated peroxidase regurgitation, but did not alter the rate of transferrin recycling. Taken together, these data indicate that, in v-Src-transformed fibroblasts, macropinocytosis and micropinocytosis serve different pathways and that cyclic AMP affects neither micropinocytosis nor the formation of macropinosomes, but selectively promotes regurgitation therefrom.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1990

Involvement of cyclic AMP in multiple, excitatory actions of biogenic amines on the cardiac ganglion of the horseshoe crab Limulus polyphemus.

Cyclic AMP appears to be involved in several excitatory actions of amines on neurones of the Limulus cardiac ganglion. Amines selectively increase levels of cardiac ganglion cyclic AMP with a magnitude and time course similar to that observed for amine-induced excitation of cardiac ganglion burst rate. With respect to either the physiological or biochemical effect, the apparent order of potency is octopamine greater than epinephrine approximately dopamine greater than norepinephrine. Elevation of cardiac ganglion cyclic AMP levels by octopamine or dopamine is dose-dependent and is potentiated by the phosphodiesterase inhibitor 3-isobutyl 1-methylxanthine (IBMX). Several pharmacological agents which influence cyclic nucleotide metabolism, including forskolin, IBMX and 8-substituted cyclic AMP analogues, have amine-like effects on the Limulus cardiac ganglion. These effects include increased burst rate of the isolated cardiac ganglion and decreased burst duration, interburst interval and number of spikes per burst in follower neurones. Forskolin and IBMX increase levels of cardiac ganglion cyclic AMP, and IBMX also increases cyclic GMP levels in this tissue. Amines, forskolin and IBMX have direct effects on follower neurones pharmacologically isolated from pacemaker cell input. Octopamine, forskolin and IBMX depolarize follower neurones, while dopamine hyperpolarizes these cells. Amines, forskolin and IBMX elicit burst-like potentials in follower neurones, and increase the size of evoked, unitary junction potentials recorded in cardiac muscle fibres. These pharmacological and biochemical data suggest that multiple, excitatory effects of biogenic amines on the Limulus cardiac ganglion are mediated by simultaneous increases in cyclic AMP at several loci within this neural network.

1-Methyl-3-isobutylxanthine↗
PubMed1982

Cytoprotective effect of cyclic AMP on cultured rabbit gastric cells.

A new experimental system with cultured gastric cells was developed to estimate the cytoprotective and damaging effects of drugs. The gastric cells were incubated in vitro in medium of pH 3, and their resistance to acid was determined by measuring percentage of damaged cells as a function of time. Pretreatment with 0.5 mM acetylsalicylic acid (ASA) for 24 h decreased their resistance (26%), whereas pretreatment with 0.3-3 micrograms/ml of 16,16-dimethylprostaglandin E2 (dimethyl PGE2) for 4 h increased their resistance (13-16%). The adenosine 3':5'-cyclic monophosphate (cyclic AMP) level in the cultured gastric cells was decreased by 0.5 mM ASA (30%) and increased by 0.3 microgram/ml of dimethyl PGE2 (38%) on treatment for 24 h. These changes reflect phenomena observed in the gastric mucosa, suggesting that this experimental system is valid as an in vitro model. Concentrations of 0.1 mM cyclic AMP and 0.1 mM N6, O2'-dibutyryladenosine 3':5'-cyclic monophosphate (dibutyryl cyclic AMP) were found to exert cytoprotective effects on the cells (5 and 7% increase, respectively). Furthermore, 0.1 mM cyclic AMP caused partial recovery from 0.5 mM ASA-induced decrease in resistance (ASA: 17%, ASA + cyclic AMP: 9%). These findings suggest that cyclic AMP plays a role in protection of cultured gastric cells and presumably also of gastric mucosal cells in vivo.

Animals↗
PubMed1976

Further studies of the action of cyclic AMP on the electrical and mechanical activities of intestinal smooth muscle.

Effects of externally applied cyclic AMP and other adrenergic stimulants on the electrical and mechanical activities of the cat small intestine were observed by using pressure electrodes. The electrical and mechanical activities were suppressed by cyclic AMP and beta-stimulants. Those inhibitory actions of cyclic AMP and beta-stimulants were potentiated under the treatment with caffeine, theophylline and papaverine which inhibits the phosphodiesterase activity. On the other hand, the inhibitory action of cyclic AMP and beta-stimulants was decreased in imidazole, an agent that increases phosphodiesterase activity. Exogenous applied concanavalin A, an agent that inhibits the adenyl cyclase activity, showed no observable changes in both activities but the effects of beta-stimulants were decreased after treatment with concanavalin A. No obvious changes on both activities were obtained in cyclic GMP and dibutyryl cyclic GMP. These findings tentatively support the hypothesis that cyclic AMP is a second messenger in the inhibitory responses to beta-stimulants on the intestinal smooth muscle. However, it is also concluded that the inhibition of mechanical activity caused by cyclic AMP is partially due to suppression of the membrane activity.

Adenylyl Cyclase Inhibitors↗
PubMed1976

Effect of adrenergic agonists on the cyclic AMP level in the liver and heart from normal and hypothyroid rats.

In order to clarify the mechanism of the different sensitivity of the adrenoceptors between normal and hypothyroid rats, cyclic AMP levels in the liver and heart were measured after the administration of phenylephrine, isoproterenol, epinephrine and methoxamine. Cyclic AMP increased in all cases, but the extent of its increment in the heart was much less than that in the liver. Phentolamine and propranolol showed only a partial inhibition of cyclic AMP elevation by the agonists in the liver from normal and hypothyroid rat. On the other hand, propranolol blocked completely the effect of the agonists on the heart from both groups. It was also observed that cyclic AMP increased in adrenalectomized rats after the injection of the adrenergic agonists. The basal activity of protein kinase in hypothyroid status was slightly lower than that in the normal, but this enzyme was stimulated in the presence of cyclic AMP in vitro. These results suggest that the function of beta-adrenoceptor remained normal even in hypothyroidism and responded well to isoproterenol and epinephrine. It is also indicated that the increased sensitivity of alpha-adrenoceptor to phenylephrine in the hy pothyroid atria previously observed is probably in part independent of the mechanism mediated by cyclic AMP.

Adrenalectomy↗
PubMed1980

Effects of alpha- and beta-adrenergic blockers on chlorpromazine-induced elevation of plasma glucose and cyclic AMP in fed mice.

The subcutaneous administration of chlorpromazine (CPZ) caused a dose response increase in plasma glucose and cyclic AMP levels in fed male mice. Hexamethonium abolished the elevation of both plasma glucose and cyclic AMP. Propranolol did not inhibit the elevation of plasma glucose but inhibited the increase of plasma cyclic AMP. In contrast, phentolamine and yohimbine completely suppressed the elevation of plasma glucose but not that of plasma cyclic AMP. These results indicate that the hyperglycemia due to CPZ was mediated through the stimulation of alpha-adrenoceptor and on the contrary CPZ increased plasma cyclic AMP through the stimulation of beta-adrenoceptor and that the increase in plasma glucose induced by CPZ was independent of the activation of adenylate cyclase and the increased plasma cyclic AMP. In addition, in contrast to phentolamine and yohimbine, phenoxybenzamine was ineffective to prevent the hyperglycemia induced by CPZ. Moreover, a higher dose of dihydroergotamine was required to inhibit the hyperglycemia.

Adrenergic alpha-Antagonists↗
PubMed1976

Changes in cyclic AMP level of rat thyroid by acute and chronic stimulation of thyrotropin in vivo.

To assess a possible postmortem change in the level of cyclic AMP, the thyroids were snap-frozen at various time intervals after removal. Rats were fed a low-iodine diet (LID) with PTU for 2 weeks and a week after PTU discontinuation (PTU withdrawal). In all cases, the cyclic AMP level tended to increase as time elapsed from removing till fixing the thyroids, but in the PTU withdrawal group, the level was rapidly increased 2-fold after 5 min. In an acute experiment, the thyroids were removed under anesthesia and frozen rapidly. Intravenous administration of ovine thyrotropin (250 mU) and TRH (500 ng) brought about a rapid increase in the thyroidal level of cyclic AMP to 40% to 20% over the control level. Two weeks after PTU treatment, circulating thyrotropin was increased to a maximum of 19-fold and a further enhancement ("rebound") was observed after PTU withdrawal. PTU treatment led to an increase in the thyroidal level of cyclis AMP pre mug DNA to 60% over the control value. Following PTU withdrawal, the rise in the level of cyclic AMP returned to the normal level. However, there was no change in the concentration when it was expressed as per mg wet tissue weight. Therefore, the increase in the thyroidal concentration of cyclic AMP per mug of DNA may be due to an increase in volume of the follicular cells.

Animals↗