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PubMed1989

Effects of sodium salicylate on the febrile response and increased levels of cyclic AMP in cerebrospinal fluid during endogenous pyrogen-induced fever in rabbits.

To further evaluate the causality between endogenous pyrogen (EP)-induced fever and cyclic adenosine-3',5'-monophosphate (cyclic AMP) level, the effects of sodium salicylate (SS) on the febrile response and increased levels of cyclic AMP in both cerebrospinal fluid (c.s.f.) and plasma during EP-induced fever in rabbits were observed. The results suggest that cyclic AMP is probably involved in the central mediation of EP-induced fever and that increased concentration of cyclic AMP in c.s.f. associated with EP-induced fever is not the result of temperature elevation but appears to be caused by the increased synthesis in the central nervous system. In addition it is confirmed that blood is impossibly a contributory source of increased cyclic AMP in c.s.f. during EP fever, and that SS may act subsequent to the increase in cyclic AMP.

Animals↗
PubMed1987

Does the positive inotropic action of a novel cardiotonic agent, MCI-154, involve mechanisms other than cyclic AMP?

MCI-154 is a new positive inotropic agent with vasodilating property. Experiments were carried out in the canine isolated right ventricular muscle in order to elucidate whether or not cyclic AMP is involved in the positive inotropic effect (PIE) of MCI-154. MCI-154 (10(-7) to 10(-4) M) produced a concentration-dependent PIE amounting to 75% of the maximal effect of isoproterenol. MCI-154 did not affect the time to peak tension and had a tendency to shorten the relaxation time and total duration of contraction. Pindolol, reserpine-pretreatment or tetrodotoxin did not modify the PIE of MCI-154. MCI-154 increased the cyclic AMP levels only at 3 X 10(-4) M, whereas CI-914, of which chemical structure is similar to that of MCI-154, elevated definitely the cyclic AMP at the lower concentrations (10(-5) to 10(-4) M). Carbachol at a concentration known to decrease markedly the PIE of amrinone, milrinone and papaverine, did not affect the PIE of MCI-154. MCI-154 inhibited the activity of a crude phosphodiesterase (PDE) from the canine ventricular muscle and it enhanced the PIE of isoproterenol, which implied the involvement of cyclic AMP. However, the maximal inhibition of PDE by MCI-154 remained less than 18%. Amrinone, milrinone and papaverine inhibited more potently the PDE activity than MCI-154. These results suggest that the elevation of cyclic AMP levels is only partially involved in the PIE of MCI-154 in the canine right ventricular muscle, and that MCI-154 may have novel mechanisms of action different from those of amrinone, milrinone and CI-914 that are largely cyclic AMP-dependent.

Animals↗
PubMed1987

Co-regulation of tracheal tone by cyclic AMP- and cyclic GMP-dependent mechanisms.

The regulation of guinea pig tracheal muscle tone by cyclic AMP-dependent and cyclic GMP-dependent relaxant mechanisms was investigated by studying the tracheal relaxant activities of forskolin, nitroprusside, N6-2'-O-dibutyryl-cyclic AMP and 8-bromoguanosine-cyclic GMP. In carbachol (3 X 10(-6) M)-contracted isolated tracheal rings, N6-2'-O-dibutyryl-cyclic AMP and 8-bromoguanosine-cyclic GMP each caused biphasic relaxation responses, which consisted of an acute relaxation followed by a sustained but lesser degree of relaxation. The biphasic nature of this response is suggested to result from a functional counter-balancing of cyclic nucleotide-dependent relaxant mechanisms and the contractile mechanisms stimulated by carbachol. The sensitivity of carbachol-contracted tracheal rings to forskolin and nitroprusside (activators of adenylate and guanylate cyclase, respectively) was generally not influenced by N6-2'-O-dibutyryl-cyclic AMP or 8-bromoguanosine-cyclic GMP in concentrations that induced up to 50% relaxation of the trachea. Furthermore, the partial relaxation of tracheal tension with one cyclic nucleotide analog did not alter the sensitivity of the tracheal rings to the other. These results demonstrate that cyclic AMP- and cyclic GMP-dependent mechanisms induce relaxations of the trachea that are functionally additive, each neither potentiating nor depressing the effects of the other. In the presence of 3 X 10(-6) M carbachol, the effectiveness of cyclic AMP- and cyclic GMP-dependent relaxant mechanisms appears to be fixed, and independent of the amount of active tension being maintained by the tracheal muscle itself.

Animals↗
PubMed1985

Receptor (norepinephrine), P-site (2',5'-dideoxyadenosine), and calcium-mediated inhibition of prostaglandin and forskolin-activated cyclic AMP-generating systems in human platelets.

Prostaglandin D2, 2-chloroadenosine, forskolin and combinations of these agents increase cyclic AMP-levels in intact human platelets. The inhibition of activated cyclic AMP-generating systems by 1) alpha2-adrenergic receptor-mediated hormonal input (norepinephrine), 2) a P-site agent (2',5'-dideoxyadenosine) and 3) a divalent cation (calcium) were examined: 1) Norepinephrine produces non-competitive inhibition of both forskolin and prostaglandin D2(PGD2)-stimulated cyclic AMP-accumulation in intact human platelets. The Ki values for norepinephrine versus forskolin, PGD2 and 2-chloroadenosine are similar in magnitude, while the Ki versus a forskolin-PGD2 combination is approximately 10-fold greater. Onset of inhibition by norepinephrine of the PGD2-response is several fold faster than for the forskolin-response. When platelets stimulated by the forskolin and PGD2 combination are exposed to norepinephrine, there is a transient increase in levels of cyclic AMP due to the potentiation of a minor beta-adrenergic component. This stimulation is followed by inhibition. 2) 2',5'-Dideoxyadenosine produces a non-competitive inhibition of the forskolin-response with a Ki of 110 microM. The inhibition of the PGD2-response by 2',5'-dideoxyadenosine is competitive with a Ki of 6-13 microM, while inhibition of the forskolin-PGD2 response has a Ki of 30 microM. Onset of inhibition by 2',5'-dideoxyadenosine is identical for forskolin or PGD2-stimulated platelets. There is a lag period for inhibition of platelets stimulated with the forskolin-PGD2 combination. The PGD2-forskolin combination appears to stabilize the cyclic AMP-generating system of platelets against inhibition by either norepinephrine or 2',5'-dideoxyadenosine. 3) Calcium ions cause a similar inhibition of cyclic AMP-generation in intact platelets, regardless of the type of stimulation.

Adenylyl Cyclase Inhibitors↗
PubMed1986

Effect of temperature on the kinetics of the yeast AMP deaminase.

The temperature dependence of the kinetics of the yeast AMP deaminase was examined using the purified enzyme and the permeabilized yeast cells. The increase in the enzyme affinity for the substrate AMP was accompanied by the decrease in the maximal velocity with the decreasing temperature in the absence and presence of ATP. The apparent Km for AMP was lowest at 15-20 degrees C, and the affinity was decreased below and above this temperature. The rate of the AMP deaminase reaction remained constant over a wide range of temperature in the presence of physiological AMP concentrations. The temperature dependent change in kinetic properties of AMP deaminase may contribute to the control of the yeast glycolytic flux under the condition of lower temperature environments.

AMP Deaminase↗
PubMed1984

Impaired plasma cyclic AMP response to exogenous glucagon in acute liver injury.

The response of plasma cyclic AMP to glucagon was investigated in 18 patients with acute liver injury to determine its value as a marker for the severity of the hepatic damage. We also investigated the interrelationship between plasma cyclic AMP response and the hyperglucagonemia often seen in this disease. Plasma cyclic AMP response to glucagon was reduced significantly in patients with acute hepatitis, particularly in severe cases with bridging hepatic necrosis. There was a significant negative correlation between log (peak % cAMP) and prothrombin time (r = -0.715, p less than 0.01), and also total bilirubin (r = -0.819, p less than 0.01). In fatal cases, the early phase of plasma cyclic AMP response after glucagon stimulation was blunted. In patients with acute liver injury, basal IRG levels were significantly high and a significant negative correlation was found between log (peak % cAMP) and basal IRG levels (r = -0.816, p less than 0.01). Our results suggest that the response of plasma cyclic AMP to exogenous glucagon could be useful in evaluating the severity of acute liver injury. The lower cyclic AMP response may be attributed to reduced hepatic reserve and endogenous hyperglucagonemia.

Acute Disease↗
PubMed1984

Muscarinic cholinergic receptors of two cell lines that regulate cyclic AMP metabolism by different molecular mechanisms.

The attenuation of cyclic AMP accumulation occurs by different mechanisms in 1321N1 astrocytoma cells and NG108-15 neuroblastoma X glioma cells. In 1321N1 cells, cholinergic agonists reduce cyclic AMP accumulation through a Ca2+-dependent activation of phosphodiesterase; in NG108-15 cells, muscarinic receptor-mediated effects on cyclic AMP metabolism occur through inhibition of adenylate cyclase. The goal of the current study was to determine whether different pharmacological specificities were expressed by the muscarinic receptor populations of these two cell lines. The affinity of muscarinic receptors for [3H]quinuclidinyl benzilate (6 pM), [3H]N-methylscopolamine (50 pM), and atropine (80 pM) was similar in membrane preparations from each cell line. The affinity of the antagonist, pirenzepine, which has been proposed to be a selective ligand for a muscarinic receptor subtype, was 3-fold higher in competition binding assays carried out with membranes of 1321N1 cells, than with NG108-15 cells. The Hill coefficients of pirenzepine competition curves were not significantly different from unity in both cell lines. This selectivity of pirenzepine was also apparent in studies of the competitive inhibition of carbachol-induced attenuation of cyclic AMP accumulation in intact cells. Differences in the relative affinities of agonists were observed in competition binding analyses carried out with membranes in the presence of GTP and absence of Mg2+. The Ki values of bethanechol and carbachol were 5- and 12-fold lower for receptors of NG108-15 cells than those of 1321N1 cells and the Ki of methacholine was 3.5-fold lower for 1321N1 cells than for NG108-15 cells. The affinities of oxotremorine and arecoline were similar between the two cell lines. These differences in agonist affinities between the two cell lines were much smaller in analyses of muscarinic receptor-mediated effects on cyclic AMP metabolism in intact cells. Taken together, these data suggest that muscarinic receptors of differing pharmacological specificities regulate cyclic AMP metabolism by different mechanisms in 1321N1 and NG108-15 cells.

Animals↗
PubMedDate not supplied

Forskolin, but not alcohol, counteracts desensitization of cyclic AMP accumulation to beta-adrenergic stimulation in rat parotid.

Forskolin at concentrations of 10 microM and above stimulates cyclic AMP accumulation in rat parotid slices. At concentrations as low as 0.1 microM forskolin also markedly potentiates the effect of isoproterenol in cyclic AMP accumulation, doing so with only slight effect on isoproterenol potency. Organic solvents such as 1-propanol are also known to potentiate the effect of isoproterenol on cyclic AMP accumulation in this tissue, although by itself propanol has little effect (2,3). The unpotentiated effect of isoproterenol is to produce only transient stimulation of cyclic AMP accumulation: Within 30 min after addition of isoproterenol cyclic AMP accumulation is nearly completely desensitized to further effects of the agonist (2). Such desensitization already established to isoproterenol (1 microM) is counteracted by 1 microM or 100 microM forskolin but not by 0.1 microM forskolin or any concentration of 1-propanol. Forskolin (1 microM or greater) potentiates isoproterenol stimulated cyclic AMP accumulation to the same degree, and at the same initial rate, in parotid tissue regardless whether it had been desensitized by pre-exposure to isoproterenol. Although 0.27 M 1-propanol potentiates the acute (2 min) 1 microM isoproterenol response to approximately the same extent as does 1 microM forskolin, no concentration of 1-propanol counteracts desensitization to isoproterenol.

1-Propanol↗
PubMed1983

Role of cyclic AMP in adrenergically-induced tracheal muscle relaxation.

Studies were performed on the isolated bovine tracheal muscle preparation to assess the possible role of adenosine 3',5'-cyclic monophosphate (cyclic AMP) in adrenergically-induced smooth muscle relaxation. Isoproterenol, epinephrine, terbutaline and soterenol were found to relax the tracheal muscle and to increase its cyclic AMP content. The two events generally paralleled one another when analyzed in terms of dose-response and time-response relationships. Propranolol antagonized the relaxation and the increase in cyclic AMP produced by isoproterenol. However, other findings suggested that there may not be a cause and effect relationship between the biochemical and mechanical responses. Thus, salbutamol and carbuterol failed to increase muscle cyclic AMP even in concentrations which produced maximum relaxation. Additionally, butoxamine and H35/25 antagonized the biochemical response but had additive effects (instead of antagonistic effects) on the mechanical response to isoproterenol. Furthermore, it was observed that low concentrations of H35/25 produced tracheal muscle relaxation associated with an increase in tissue cyclic AMP; however, use of a high concentration of H35/25 paradoxically resulted in autoblockade of the increase in cyclic AMP but not the smooth muscle relaxation.

Adrenergic alpha-Agonists↗
PubMed1980

Potentiation of cholera toxin-stimulated cyclic AMP production in cultured cells by inhibitors of RNA and protein synthesis.

Cyclic AMP increased 8- to 10-fold after a 3-h treatment with 6 nM cholera toxin in rat C6-2B astrocytoma cells. In the presence of cycloheximide, cholera toxin increased intracellular cyclic AMP about 50-fold. Qualitatively similar potentiation of cholera toxin action by cycloheximide was observed in isolated swine aortic vascular smooth muscle cells. Cycloheximide, by itself, had no effect upon cyclic AMP levels and did not alter the apparent Ka for cyclic AMP generation by cholera toxin in the cells. Also, cycloheximide did not appear to augment cholera toxin action via inhibition of cyclic nucleotide phosphodiesterase. Puromycin and actinomycin D also augmented cholera toxin action in C6-2B cells. Potentiation of cholera toxin-increased cyclic AMP formation by cycloheximide was correlated with the inhibition of [14C]leucine incorporation into protein. These results indicate that the ability of cholera toxin to stimulate cyclic AMP production in C6-2B astrocytoma and swine vascular smooth muscle cells is enhanced by inhibition of de novo protein synthesis.

1-Methyl-3-isobutylxanthine↗
PubMed1982

Enzymatic regulation of mast cell activation and secretion by adenylate cyclase and cyclic AMP-dependent protein kinases.

This review details the biochemical events that follow IgE dimerization by antigen and cross-linking of receptors and are linked with the early rise in cyclic AMP. That the monophasic rise in cyclic AMP at 15 s is essential to the degranulation process is evident by pharmacological manipulation of adenylate cyclase, using specific activators and inhibitors to achieve potentiation and inhibition of immunologic release, respectively. Although only a small percentage of membrane adenylate cyclase is transmembrane linked to IgE-Fc perturbation, its product, cyclic AMP, is elevated during activation and is responsible for the activation of two protein kinase isoenzymes at 30-60 s. This sequence appears to be essential for secretion to occur, as evidenced by dose-related inhibition of both beta-hexosaminidase release and protein kinase activation by adenylate cyclase inhibitors. Competitive activation of cyclic AMP-dependent protein kinase activity by a phosphodiesterase inhibitor leads to inhibition of mediator release by diverting an essential enzyme or recruiting an inhibitory sequence. The precise functional role of the mast cell cyclic AMP-dependent protein kinases has not yet been identified, but there is much evidence in other cell types that protein phosphorylation is an essential accompaniment to cellular regulation. Although other apparently essential biochemical steps are noted, such as uncovering a serine esterase, methylation of membrane phospholipid, and increased Ca2+ influx, only a portion of the activation-secretion response is presented here as a sequence, namely, the IgE-Fc receptor-initiated, transmembrane-coupled activation of adenylate cyclase and the subsequent cytoplasmic cyclic AMP-dependent activation of types I and II protein kinases.

Adenylyl Cyclases↗
PubMed1980

The effect of lithium on noradrenaline-induced cyclic AMP accumulation in rat brain: inhibition after chronic treatment and absence of supersensitivity.

Lithium (Li) has been reported to inhibit numerous adenylate cyclases, but often these reports used clinically toxic concentrations of Li and their relevance to a theory of Li action was questionable. The present report demonstrated Li inhibition beginning at 2 mM of the norepinephrine (NE)-induced cyclic AMP accumulation in a resuspended P2 pellet containing intact synaptosomes and in slices from rat cortex. The inhibition is demonstrable with isoproterenol as well and in the presence of a phosphodiesterase inhibitor. In cortical slices removed from rats treated for 21 days with therapeutically equivalent Li serum levels, NE-induced cyclic AMP accumulation is inhibited by over 70%. After cessation of 21 or 42 days of Li treatment, an enhancement of cyclic AMP accumulation to NE is not demonstrable. Rubidium and cesium do not inhibit NE-induced cyclic AMP accumulation. These ions cause an increase in basal cyclic AMP accumulation in the absence of NE, as does Li to a lesser degree. The effect of Li to inhibit NE-induced cyclic AMP accumulation is therefore specific to the Li ion, occurs at therapeutically equivalent concentrations, continues after chronic treatment and does not cause a compensatory supersensivity in the manner of the NE-receptor blocking drugs.

4-(3-Butoxy-4-methoxybenzyl)-2-imidazolidinone↗
PubMed1980

Further studies on the effect of cholecystokinin and secretin on the content of cyclic AMP, cyclic GMP, protein and calcium in pure pancreatic juice of dogs.

The present work deals with the time course of pancreatic secretion of cyclic AMP, cyclic GMP, calcium and protein in response to cholecystokinin (CCK) and secretin (S). Three dogs with gastric and duodenal Thomas cannulae were given 1 Clinical Unit/kg/h of secretin for 150 min. CCK was added to the infusion after the first 75 min. Only one dose of CCK (0.75, 1.5, 3, 6, 16 24 Ivy dog U/kg/h) was given in any one experiment. Pancreatic juice was collected at one minute intervals for the first 15 min. at the beginning of the CCK infusion and at 15 min. intervals thereafter. CCK induced a biphasic pattern of pancreatic secretion: within 3 to 10 min. flow rate, protein, calcium, cyclic AMP and cyclic GMP output peaked in a dose dependent parallel manner. Then, the maximal flow remained constant while protein output reached a steady state; its value was fairly similar to that of the early peak for 0.75 to 6 U and for 16 and 24 U, the steady state value was lower than the first peak value. The pattern of calcium output was similar to that of protein output. The output of cyclic AMP and cyclic GMP increased until the end of the CCK infusion. When CCK (3 U/kg) was given as an intravenous bolus injection without any background of secretin, cyclic AMP, cyclic GMP and protein outputs peaked within 3 min. and then decreased. The results show that not only calcium and protein but also cyclic AMP and cyclic GMP secretion in the pancreatic juice depends on CCK. Key words: Dog, secretin, cholecystokinin, pancreatic juice: cyclic AMP, cyclic GMP, calcium, protein.

Animals↗
PubMed1980

Plasma cyclic AMP levels in response to exercise and terbutaline sulphate aerosol in normal and asthmatic subjects.

A study was performed to investigate changes in plasma cyclic adenosine monophosphate (cyclic AMP), peak expiratory flow and arterial blood gas tensions in response to running exercise and terbutaline sulphate aerosol in asthmatic patients regularly receiving sympathomimetic bronchodilator aerosols. Seven normal subjects were controls. Placebo aerosol was administered 20 min before the first exercise study and 1.0-1.25 mg terbutaline sulphate substituted 20 min after the first test and again 20 min before the second test. Blood gas tensions, expiratory flow and cyclic AMP were measured at rest, during and after exercise. Exercise induced a significant increase in cyclic AMP in both asthmatic and normal subjects. The change in plasma levels was not significantly different between groups. Cyclic AMP values were higher at rest and during exercise with terbutaline sulphate compared with placebo for both groups. Terbutaline sulphate blocked the marked fall in peak expiratory flow and arterial oxygen tension observed in the asthmatic subjects following the first test. Values for cyclic AMP following exercise were not significantly different between asthmatic and normal subjects. In contrast to other reports our asthmatics have a marked increase in cyclic AMP in response to exercise and to a beta-sympathomimetic aerosol.

Adult↗
PubMed1982

Thyrotropin-releasing hormone and cyclic AMP activate distinctive pathways of protein phosphorylation in GH pituitary cells.

The studies reported here were undertaken to clarify the cellular mechanism of the hypothalamic tripeptide, thyrotropin-releasing hormone (TRH), in clonal, hormone-responsive GH pituitary cells and to assess the possibility of a role for cyclic AMP as a mediator of TRH action. We investigated patterns of protein phosphorylation by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and autoradiography of high speed supernatant and pellet fractions from untreated and treated GH cells. Brief treatment of cells with agents which elevate or mimic cellular cyclic AMP (8-bromo cyclic AMP, dibutyryl cyclic AMP, vasoactive intestinal polypeptide or cholera toxin) stimulated the phosphorylation of five supernatant peptides (41, 45, 47, 72, and 82 kilodaltons) and one pellet peptide (135 kilodaltons) and decreased the phosphorylation of one supernatant peptide (55 kilodaltons). In contrast, TRH promoted the phosphorylation of four different supernatant peptides (two 59, 65, and 80 kilodaltons). In addition, TRH also stimulated the phosphorylation of cyclic AMP-responsive 41-, 45-, and 82-kilodalton supernatant peptides and 135-kilodalton pellet protein and decreased the phosphorylation of 55-kilodalton supernatant peptide. Altered labeling of 47- and 72-kilodalton supernatant peptides, however, was not observed with TRH. Time course studies, as well as the overlapping biological action of TRH and vasoactive intestinal polypeptide, lead us to conclude that these peptide hormones utilize distinct, parallel pathways which converge at some late step. Furthermore, the results indicate that effects of TRH are mediated by a cyclic AMP-independent pathway.

Animals↗
PubMed1982

[C-AMP concentration in various organs of female rats and in human ovaries with aging (author's transl)].

The change in 3',5'-cyclic adenosine monophosphate (c-AMP) concentration was observed in various organs of rats in gonadal cycle in adult group and with aging (30, 70, 100, 120 weeks), and in human ovaries with aging. 1) The average c-AMP concentration of ovaries of rats showed a significant change with estrus cycle and was higher in the following sequence: proestrus, diestrus II, diestrus I and estrus phase. This tendency was also seen in hypothalamus and pituitary, but was not statistically significant, 2) The average c-AMP concentration in tissues began to decline significantly from 70 weeks in cerebral cortex and hypothalamus, and from 80 weeks in ovaries. However, on the other hand the concentrations in pituitary, liver and adrenal declined markedly from 100 weeks. 3) The c-AMP in ovaries of 80 weeks rats by pregnant mare serum (PMS) road increased by 0.5-fold in concentration, and by 0.6-fold in whole tissue relative to that of 30 weeks rats. 4) A significant difference in serum LH and FSH level between ovarian artery and vein was not found in cycling mature group, non-cycling climacteric group and post-menopausal group of women. 5) Both average concentrations and total values of c-AMP in ovaries of non-cycling climacteric and post-menopausal women were lower than those of mature cycling women. This fact may imply a different response by ovarian tissues such as corpus luteum, follicle and other tissues to gonadotropin. From these results of c-AMP in tissues, it is concluded that the decline of ovarian function with aging of rats was relatively earlier than pituitary, although being delayed compared with hypothalamus, and were the ovarian function in humans declined in the premenopausal period.

Adult↗
PubMed1983

Alteration in cyclic AMP-dependent protein kinases and polyamine biosynthetic enzymes during hypertrophy and hyperplasia of the thyroid in the rat.

After 2 weeks of goitrogen treatment [propylthiouracil (PTU), 0.02% in drinking water], the thyroids of rats increased to 280% of control wet weight, 270% of dry weight, and 250% of control DNA content. Two phases of growth were apparent, an initial hypertrophy phase lasting 3 days (increase in cell size and gland weight with no detectable increase in DNA) and a hyperplastic phase (increase in DNA with histological evidence of cell proliferation) starting at 3-4 days and continuing through 14 days. The cyclic AMP-dependent protein kinase activity ratio (-cyclic AMP/+cyclic AMP) showed a biphasic pattern during the 2-week thyroid growth period, with maxima at day 1 (132% of control) and day 6 (148% of control). Ornithine decarboxylase (EC 4.1.1.17), the initial enzyme in polyamine biosynthesis, showed a similar biphasic pattern with a 6- to 7-fold elevation in activity at 2-3 days and a 4-fold elevation at 6 days. S-Adenosyl-L-methionine decarboxylase (EC 4.1.1.50), the enzyme which catalyzes spermidine synthesis, was elevated 4-fold at 9 days of treatment. The thyroid total supernatant protein kinase activity (+cyclic AMP) increased to 160% of control by 4 days, returning to control by 14 days of PTU treatment. The thyroid had 10% Type I activity and 90% Type II cyclic AMP-dependent protein kinase activity. The specific activity of both Types I and II remained unchanged for the first 2 days of PTU treatment. Both types increased to 150% of control by 4 days. Type I remained elevated throughout the remainder of the 14 days, in contrast to Type II, which decreased conspicuously to control levels by 6 days. A single injection of thyroid-stimulating hormone (TSH, 1.0 unit/100 g of body weight, i.p.) resulted in a 20-fold increase in thyroid ornithine decarboxylase activity by 4 hr. The same dose of TSH produced only a 3-fold induction of ODC in rats hypophysectomized 2 weeks previously. The thyroid specific activity of Types I and II protein kinase was only 55% and 57% of control, respectively, in these unresponsive rats. Thyroids from rats chronically stimulated for 14 days showed an increase in ornithine decarboxylase following TSH administration similar to that of control rats. Changes in the activation as well as specific activity of Types I and II protein kinase during hypertrophy and hyperplasia underlie the complexity of a cyclic AMP-mediated response.

Adenosylmethionine Decarboxylase↗
PubMed1982

[Cyclic AMP level in the muscle tissue of cattle and the physico-chemical properties of meat].

The purpose of this study was to determine quantitative changes of cyclic adenosine mono-phosphate (c-AMP) level in meat of slaughter bulls. Meat samples were taken from the muscle longissimus dorsi (LD) of bulls overstressed by transport, which were stunned with electricity without rest. The obtained data did not show statistical correlations between c-AMP level and pI-values but showed statistical correlations between c-AMP level and some sensory properties of beef. The highest concentration of c-AMP was detected in the muscle about 90 minutes after slaughter. Individual differences in the concentration of c-AMP in the LD were observed in 30 min. after slaughter. In this time the high c-AMP level was correlated with the colour and sensory properties of meat and bouillon.

Animals↗