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At least 19 recordsLinked to original sources
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↗
PubMed1991

Calcitonin gene-related peptide (CGRP) causes endothelium-dependent cyclic AMP, cyclic GMP and vasorelaxant responses in rat abdominal aorta.

Calcitonin gene-related peptide (CGRP), a neuropeptide found in nerves surrounding most blood vessels, is a potent hypotensive agent in both humans and rats. In isolated strips of rat thoracic aorta, CGRP has been reported to cause endothelium-dependent relaxation. To study the cellular and molecular mechanisms involved in CGRP-induced vasodilation, we investigated the roles of two second messengers, cyclic AMP and cyclic GMP, as potential mediators of the signal transduction mechanism leading to vasodilation in response to CGRP in rat aorta. In the present study, the abdominal aorta, rather than thoracic aorta, was used because of its higher content of endogenous CGRP and, therefore, the greater likelihood of regulation by CGRP in vivo. Each abdominal aortic ring was precontracted with norepinephrine (NE) at its EC50 concentration (10-20 nM). CGRP (3-300 nM) caused concentration-dependent relaxations (reducing the NE-induced contractions by 34%) that were completely dependent on endothelium. The relaxations in response to CGRP were correlated in a time- and concentration-dependent manner with increases in aortic levels of both cyclic AMP and cyclic GMP. CGRP (100 nM) caused significant elevations of cyclic AMP levels (1.4 to 3.2 pmol/mg protein, at 1 min) and cyclic GMP levels (1.6 to 3.6 pmol/mg protein, at 30 s). Like the vasorelaxant responses, both cyclic AMP and cyclic GMP responses to CGRP were totally dependent on the endothelium. Pre-incubation with indomethacin (3 microM, 15 min) did not alter cyclic AMP responses to CGRP (100 nM), suggesting that prostaglandins are not involved. Therefore, CGRP-induced vasodilations of abdominal aorta involve an endothelium-dependent mechanism associated with cyclic GMP elevations, similar to the mechanisms of vasodilation in response to acetylcholine and other endothelium-dependent vasodilators. However, CGRP-induced relaxations of aorta involve an additional mechanism (i.e., endothelium-dependent cyclic AMP elevations), which may also contribute to the intracellular mechanism of aortic vasodilation in response to CGRP.

1-Methyl-3-isobutylxanthine↗
PubMed1991

Calcitonin gene-related peptide (CGRP)-induced cyclic AMP, cyclic GMP and vasorelaxant responses in rat thoracic aorta are antagonized by blockers of endothelium-derived relaxant factor (EDRF).

The mechanism of CGRP-induced vasodilation in rat thoracic aorta was investigated using antagonists of the classical endothelium-derived vasorelaxant factor (EDRF) and comparisons with acetylcholine-induced vasodilations. The CGRP-induced relaxations of isolated rings of rat thoracic aorta were completely dependent on the presence of endothelium and were associated with increases in the levels of both cyclic AMP and cyclic GMP, the same as in our previous study using rat abdominal aorta. Maximum relaxations to CGRP, which represented 40-50% reversal of the norepinephrine-induced contractions, occurred with 100 nM CGRP. Addition of acetylcholine (ACh, 1 microM) to aortic rings, which were already maximally relaxed to CGRP, caused further relaxation to 100%, suggesting that CGRP may use a mechanism (or pool of EDRF) different from that of ACh. Both CGRP- and ACh-induced relaxations of aorta were significantly inhibited by the EDRF blocking agents, hemoglobin (10 microM), methylene blue (10 microM), and nordihydroguaiaretic acid (NDGA, 10 microM). In fact, hemoglobin and NDGA were more effective as inhibitors of CGRP-induced relaxations than ACh-induced relaxations. Hemoglobin, methylene blue and NDGA also inhibited the CGRP-induced increases in both cyclic AMP and cyclic GMP levels. On the other hand, indomethacin, a cyclo-oxygenase inhibitor, did not alter CGRP-induced vasorelaxations or increases in either cyclic AMP or cyclic GMP levels, suggesting that prostaglandins are not involved. Therefore, CGRP-induced vasodilations in rat thoracic aorta appear to involve EDRF, leading to cyclic GMP elevations in smooth muscle and ultimately vasorelaxations. However, another previously undescribed mechanism, which involves EDRF-dependent and indomethacin-resistant elevations of cyclic AMP levels, is triggered by CGRP in thoracic aorta. This novel EDRF-dependent cyclic AMP response may contribute to the CGRP-induced vasodilation in rat thoracic aorta.

Acetylcholine↗
PubMed1975

Cyclic AMP, cyclic GMP, and glucocorticoids as potential metabolic regulators of epidermal proliferation and differentiation.

The two cyclic nucleotides, cyclic AMP and cyclic GMP, appear to be central to the metabolic regulation of cell proliferation and differentiation in various cells. Moreover, in many systems glucocorticoids appear to act in concert with or parallel to cyclic AMP. The available evidence suggests that these three molecular species--cyclic AMP, cyclic GMP, and glucocorticoids--may be essential to the normal regulation of epidermal proliferation and differentiation. In 1970, we suggested that perturbed epidermal homeostasis, exemplified by psoriasis, might be associated with low cellular levels of cyclic AMP and, in 1972, with high levels of cyclic GMP as well. Subsequent measurements of these two cyclic nucleotides in our laboratory showed a probable reduction in the cyclic AMP/cyclic GMP ratio in lesional psoriatic tissue. This led to the hypothesis that the cardinal features of psoriatic epidermis--glycogen accumulation, excessive proliferation, and reduced cell specialization--are the results of this reduced ratio. A corollary of this hypothesis was that a psoriatic lesion could not begin or exist without this altered cyclic nucleotide ratio. Recently, four different agents--lithium, a beta adrenergic blocking agent, antimalarials, and iodide--have been found to exacerbate psoriasis and to reduce the formation of cyclic AMP in various tissues. Consequently we believe that cyclic nucleotides are of central importance in the pathogenesis of the epidermal component of psoriasis.

Animals↗
PubMed1980

Immunohistochemical localization of cyclic AMP, cyclic GMP and calmodulin in Dictyostelium discoideum.

Using an indirect immunofluorescence technique cyclic AMP, cyclic GMP and calmodulin have been localized in Dictyostelium discoideum cells. The bound cyclic AMP is localized throughout the cell. Cyclic GMP and calmodulin are markedly localized in the nuclear area of the cell. No changes in the pattern of staining was observed during differentiation. Chemotactic stimulation induced a transient increase of cyclic GMP staining.

Calcium-Binding Proteins↗
PubMed1975

Adenosine, AMP, cyclic AMP, theophylline and the action and production of erythropoietin.

Erythropoiesis, as measured by the uptake of 59Fe into plethoric mice, is stimulated by adenosine, AMP, cyclic AMP, and dibutyryl cyclic AMP, but not by cytidine, its nucleotides or cyclic GMP. This stimulation is erythropoietin dependent, because it is prevented by anti-erythropoietin. Theophylline neither stimulates erythropoiesis nor potentiates the action of erythropoietin on bone marrow cells in plethoric mice. Theophylline does potentiate the production of erythropoietin in rats following a frief hypoxic exposure but does not cause a similar increase in mice.

Adenine Nucleotides↗
PubMed1977

Effects of parathyroid hormone on cyclic AMP, cyclic GMP, and efflux of calcium in isolated renal tubules.

The effects of parathyroid hormone (PTH) on concentrations of cyclic AMP and cyclic GMP were investigated in isolated renal cortical tubules from hamsters. Efflux of 45Ca from tubules was compared to temporal changes in both cyclic nucleotide concentrations. A rapid increase in cyclic AMP occurred following addition of PTH which was maximal by 1 min but decreased over the next 4 min period. Cyclic GMP concentrations were not significantly altered at 1 min but increased between 1 and 5 min from basal levels. Concentrations of both nucleotides remained significantly elevated from basal levels between 5 and 15 min following PTH. Efflux of 45Ca was increased by PTH with time-course changes closely paralleling changes in cyclic GMP concentrations. Changes in both cyclic AMP and cyclic GMP were related to PTH concentrations of the incubation media and were increased by addition of theophylline. Increasing the calcium concentration from 1 to 3 mM did not significantly alter the effect of PTH on cyclic AMP, however, cyclic GMP concentrations were further increased.

Animals↗
PubMed1990

[In vivo biochemical aspects of adverse reactions of contrast media--sequential changes of histamine, cyclic AMP, cyclic GMP].

The effect of conventional high-osmolality contrast media (diatrizoate) and new low-osmolality contrast media (iopamidol) on plasma histamine, cyclic AMP and cyclic GMP levels have been examined in a group of 37 mongrel dogs. Plasma histamine levels have a tendency of elevation at five minutes after initiation of injection of diatrizoate and iopamidol in low dose (5 ml/kg). However, statistically no significant changes were found in either diatrizoate or iopamidol in low dose (5 ml/kg) or high dose (15 ml/kg). Plasma cyclic AMP levels have elevated significantly in twenty minutes after termination of injection of iopamidol in low dose (5 ml/kg) and in high dose (15 ml/kg). Also plasma cyclic AMP levels have elevated significantly in twenty minutes after termination of injection of diatrizoate in high dose (15 ml/kg). These findings indicate iopamidol has potential of elevating plasma cyclic AMP as compared with diatrizoate. Plasma cyclic GMP levels have elevated significantly in twenty minutes after termination of injection of diatrizoate in low dose (5 ml/kg) and in high dose (15 ml/kg). Also plasma cyclic GMP levels have elevated significantly in twenty minutes after termination of injection of iopamidol in high dose (15 ml/kg). These findings indicate diatrizoate has potential of elevating plasma cyclic GMP as compared with iopamidol. It is suggested that iopamidol has potential of elevation of plasma cyclic AMP that suppresses histamine release and diatrizoate has potential of elevation of plasma cyclic GMP that enhances histamine release. And so iopamidol is though to be minor histamine releaser than diatrizoate.

Animals↗
PubMed1976

Stimulus-secretion coupling: role of cyclic AMP, cyclic GMP and calcium in mediating enzyme (kallikrein) secretion in the submandibular gland.

1. The role of adenosine 3':5'-phosphate (cyclic AMP) and guanosine 3':5'-phosphate (cyclic GMP) as second messengers for the enzyme secretory response evoked by the autonomic neurotransmitters, noradrenaline and acetylcholine, is examined in this in vitro study on the guinea-pig submandibular gland. 2. Noradrenaline increased enzyme (kallikrein) secretion. The initial stimulation of enzyme release appeared to be dose-dependent. The time course of cumulative kallikrein secretion revealed a complex pattern. Isoprenaline and phenylephrine were almost as potent as noradrenaline in releasing kallikrein. Both propranolol and phentolamine were required to fully inhibit the noradrenaline-stimulated enzyme secretion. 3. The cumulative secretion of kallikrein evoked by acetylcholine was dose-dependent. The onset of secretion showed a significantly greater time-lag than that observed with noradrenaline. Atropine effectively blocked the release of kallikrein by acetylcholine. 4. Dibutyryl cyclic AMP stimulated enzyme secretion. Dibutyryl cyclic GMP caused an initial increase which was not maintained. 5. The cyclic nucleotide phosphodiesterase inhibitors, theophylline and papaverine, increased basal kallikrein secretion. The action of the cyclic phosphodiesterase inhibitors on the secretory response to noradrenaline, acetylcholine, dibutyryl cyclic AMP and dibutyryl cyclic GMP was complex. In general, the increase in enzyme release produced by the secretagogues was additively enhanced by both inhibitors. 6. Omission of calcium inhibited both acetylcholine and dibutyryl cyclic GMP stimulated kallikrein release, but to a lesser degree than that of noradrenaline and dibutyryl cyclic AMP. High concentrations of extracellular calcium (10 mM) appeared to enhance the action of acetylcholine. 7. Noradrenaline produced a rise in the intracellular level of cyclic AMP. The increase preceded the stimulated secretion of kallikrein. Of the various adrenergic agonists, noradrenaline and isoprenaline were the most potent, whereas phenylephrine was significantly less effective in raising basal cyclic AMP values. Acetylcholine was without effect, even in the presence of a cyclic phosphodiesterase inhibitor. 8. Acetylcholine and noradrenaline raised intracellular levels of cyclic GMP only when the tissue incubations were performed in the presence of a cyclic phosphodiesterase inhibitor. The increase in cyclic GMP produced by acetylcholine preceded enzyme secretion. 9. Morphological data substantiated the finding that the in vitro release of kallikrein evoked by the secretagogues was associated with the depletion of secretory granules and vacuolations in acinar cells of the gland slices. 10. The molecular mechanisms which control enzyme secretion in the exocrine submandibular gland are discussed. Models are presented for the role of transmitter-specific cyclic nucleotides and calcium in stimulus-secretion coupling.

Acetylcholine↗
PubMed1994

Cross talk among cyclic AMP, cyclic GMP, and Ca(2+)-dependent intracellular signalling mechanisms in brain capillary endothelial cells.

C-type natriuretic peptide and sodium nitroprusside, a nitric oxide donor molecule, induced large increases in cyclic GMP formation in cultured rat brain capillary endothelial cells. Isoproterenol, a potent agonist of adenylate cyclase, potentiated the actions of C-type natriuretic peptide and of sodium nitroprusside. These actions were not observed in the presence of isobutylmethylxanthine and were mimicked by forskolin. Endothelin-1 had no action on basal cyclic GMP levels. It reduced cyclic GMP formation induced by C-type natriuretic peptide and sodium nitroprusside by about 50%. These actions involved an ETA receptor subtype and a Ca(2+)-dependent and protein kinase C-independent mechanism. Finally, increasing cyclic GMP slightly prolonged intracellular Ca2+ transients induced by endothelin-1. The results suggest the presence of extensive cross talk among cyclic AMP, cyclic GMP, and Ca(2+)-dependent mechanisms in endothelial cells of brain microvessels. The relevance of the results to the regulation of the blood-brain barrier permeability is discussed.

1-Methyl-3-isobutylxanthine↗
PubMed1991

Potentiation by a sodium channel activator of effects of lithium ion on cyclic AMP, cyclic GMP and inositol phosphates.

The effects of the lithium ion (Li+) on receptor-mediated synthesis of second messengers were determined, when cellular sodium channels were quiescent or excited, using the murine neuroblastoma clone (N1E-115). In this clone, lithium inhibited the receptor-mediated synthesis of cyclic AMP and cyclic GMP and it also increased the accumulation of inositol phosphates by a receptor-mediated process. When veratridine (20 microM) excited the sodium channel, the effects of lithium were potentiated. However, tetrodotoxin, a sodium channel blocker, completely prevented this potentiation. These results suggest that when neurons are depolarizing actively and intraneuronal levels of lithium increase by entry through the sodium channel, lithium has a more potent intracellular effect. As a result, lithium would have more potent and selective effects in those pathologically-active neurons underlying manic-depressive disorder.

Animals↗
PubMed1992

[Circadian changes of atrial natriuretic peptide, cyclic AMP, cyclic GMP, sodium, blood pressure and heart rate in normal subjects].

To investigate the circadian change in the plasma atrial natriuretic peptide (ANP) concentrations and its relation to cyclic AMP (cAMP), cyclic GMP (cGMP) and serum sodium. This investigation was conducted on 22 normal subjects consisting of 16 men and 6 women with a mean age of 21.5 years. Blood samples, systolic blood pressure (SBP), and heart rate (HR), were collected and recorded every 8 hours during a 24 hour period. SBP and HR were highest at 1600 h (p less than 0.05). Plasma ANP concentrations at 0800 h (196.3 +/- 140.6 ng/L, p less than 0.01) and 1600 h (203.4 +/- 127.5 ng/L, p less than 0.01) were higher than at 2400 h (64.4 +/- 46.0 ng/L). Serum sodium, plasma cAMP, and cGMP were at the highest level at 1600 h (p less than 0.05). Plasma ANP correlated with plasma cAMP, cGMP, serum sodium, SBP, and HR (r = 0.378 - 0.419, p less than 0.05). This data supports the assumption that atrial wall distension seems to be a stimulus for ANP release.

Adolescent↗
PubMed1981

Relationship among isoproterenol, cyclic AMP, cyclic AMP-dependent protein kinase and lipolysis in perfused fat cells.

By using perfused fat cells the effect of isoproterenol on adenosine 3':5'-monophosphate (cAMP) levels, cAMP-dependent protein kinase activity and lipolysis was studied. An infusion of isoproterenol (10(-7) M) resulted in a time-dependent increase in cAMP levels and protein kinase activity in the fat cells. Both parameters reached maximum values after 5 min of drug infusion, then declined to steady-state values by 10 min. At 60 min, cAMP levels were still significantly (P less than .05) elevated over basal. Dose-response curves were determined for isoproterenol on cAMP levels, protein kinase activity and glycerol release. All three parameters were increased by isoproterenol over the same concentration range (10(-9)--10(-7) M). A plot of cAMP levels or protein kinase activity ratios vs. glycerol release resulted in linear relationship with high degrees of correlation (r = 0.98). The rates at which cAMP levels and glycerol release decline after termination of isoproterenol infusion were studied. Half-life values of 5.8 and 6.9 min were obtained for cAMP levels and glycerol release, respectively. These results support the hypotheses that cAMP, acting through protein kinase, is an intracellular mediator of the lipolytic response to isoproterenol. It is concluded that cAMP is not formed in great excess of that necessary to maximally increase lipolysis.

Adipose Tissue↗
PubMed1980

[In vitro effects of glycolytic substrates and some nucleotides (ATP, ADP, AMP, cyclic AMP) on the motility of spermatozoids of human sperm, asthenospermic or normal].

The effects of several drugs upon normal and asthenospermic human sperms were tested: cyclic AMP significantly and constantly increased the rate of motile spermatozoa in most samples having an initial motility rate between 20 and 60%. ATP kept up high the motility rate, particularly in sperm displaying the highest initial motility. Other drugs (glycolytic substrates, pyruvate, ADP, AMP, caffeine had inconstant effects upon a few sperms. None drug was efficient upon sperms with initial motility rate lower than 20%; this was probably due to important lesions of the locomotor apparatus of the spermatozoa, as shown by electron microscopy investigations.

Adenine Nucleotides↗