Effects of Cyclic Adenosine Monophosphate and Melanocyte-Stimulating Hormone on Frog Skin In Vitro

Nature ◽  
1965 ◽  
Vol 208 (5017) ◽  
pp. 1282-1284 ◽  
Author(s):  
M. W. BITENSKY ◽  
S. R. BURSTEIN
Keyword(s):  
Frog Skin ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Melanocyte Stimulating Hormone ◽  
Stimulating Hormone

Effects of hormones on 3', 5' -cyclic adenosine monophosphate in choroid plexus.

1977 ◽  
Vol 232 (4) ◽  
pp. E353
Author(s):  
D Rudman ◽  
B M Hollins ◽  
N C Lewis ◽  
J W Scott
Keyword(s):  
Effective Dose ◽  
Choroid Plexus ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Tyrode Solution ◽  
Minimal Effective Dose ◽  
Camp Content ◽  
Melanocyte Stimulating Hormone ◽  
Stimulating Hormone

Choroid plexus of rabbit and rat was incubated for 2-30 min at 37 degrees C under 95% O2-5% CO2 in Tyrode solution containing 10 mM glucose and 1 mM theophylline with these agents: epinephrine, norepinephrine, isoproterenol, dopamine, histamine, serotonin, arginine, and lysine vasopressins, oxytocin, angiotensin, adrenocorticotropin (ACTH), beta-melanocyte-stimulating hormone, and choroid plexus peptide IIF. After incubation, tissue and medium were analyzed for 3', 5' -cyclic adenosine monophosphate (cAMP) content. Each amine or peptide was tested initially at 1,000 microng/ml. Only ACTH and serotonin affected cAMP content of rabbit choroid plexus. At 1,000 microng/ml, these agents caused a 10 and 4 times (respectively) increase in cAMP content of tissue + medium at 2-10 min with decline in content at 10-30 min. More than 90% of the increment was located in tissue, less than 10% in medium. Minimal effective dose (MED) to cause a significant (P less than .05) accumulation of cAMP was 0.1 microng/ml (2.2 x 10(-8) M) for ACTH and 10 microng/ml (5.7 x10(-3) M) for serotonin. Only isoproterenol, epinephrine, and norepinephrine influenced cAMP content of rat choroid plexus. MED's for this effect by isoproterenol, epinephrine, and norepinephrine were .001, .01, and 10 microng/ml (4.7 x 10(-9), 5.5 x 10(-8), and 5.9 x 10(-5) M), respectively.

MELANOCYTE STIMULATING HORMONE INHIBITION BY ACETYLCHOLINE AND NORADRENALINE IN THE FROG SKIN BIOASSAY

1966 ◽  
Vol 51 (1) ◽  
pp. 149-160 ◽  
Author(s):  
Halvor Möller ◽  
Aaron B. Lerner
Keyword(s):  
Frog Skin ◽  
Rana Pipiens ◽  
Individual Response ◽  
Melanocyte Stimulating Hormone ◽  
Skin Samples ◽  
Stimulating Hormone

ABSTRACT The mechanism of aggregation induced in MSH-dispersed dermal melanocytes was studied in Rana pipiens by reflectance photometry in vitro and by microscopy in vivo. Acetylcholine inhibits MSH strongly and irreversibly in one third of all frogs tested in vitro and has almost no effect on the remaining animals. No lightening action occurs in vivo. Different skin samples from the same animal give the same response to acetylcholine. An individual response to acetylcholine implies similar responses to other cholinergics. The lightening action of acetylcholine is inhibited by atropine. Noradrenaline induces a reversible MSH-inhibition in all frogs in vitro as well as in vivo. The lightening action of noradrenaline, inhibited by sympatholytics, is ten times stronger than that of acetylcholine. The l-isomer has only twice the lightening potency as the d-isomer. Both lightening agents work if given at the maximum of MSH-dispersion or before the addition of MSH. Fundamental differences between the mechanisms of dispersion and aggregation, and between the lightening induced by acetylcholine and by noradrenaline, are emphasized.

scholarly journals ID: 1069 Effect of Diutyryl-CAMP and follicle stimulating hormone on in vitro maturation of porcine oocyte

2017 ◽  
Vol 4 (S) ◽  
pp. 151
Author(s):  
Nguyen Thi Thuy Van ◽  
Pham Truong Duy ◽  
Nguyen Van Thuan ◽  
Bui Hong Thuy
Keyword(s):  
In Vitro Maturation ◽  
Follicle Stimulating Hormone ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Treated Group ◽  
Cell Stage ◽  
Cumulus Expansion ◽  
Stimulating Hormone

In this study, we examine the effects of dibutyryl cyclic adenosine monophosphate (dbcAMP) and follicle stimulating hormone (FSH) on the maturation of nucleus and cytoplasm of porcine oocytes after in vitro maturation. The oocytes-granulosa cell complexes (OCGs) were cultured in three different maturation media: basic, basic+dbcAMP, and basic+dbcAMP+FSH to investigate the cumulus expansion and maturation of the fully-grown oocytes. Treated mature oocytes underwent parthenogenetic activation to examine the quality of the mature oocytes via the development of embryos. The results showed that there was a higher rate of cumulus expansion and maturation between the combination of dbcAMP and FSH group (95.1% and 85.3%) compare with the none treatment or only dbcAMP treated group (40.8% and 47.7%; 44.9% and 42.9% respectively). The results in embryos development showed that mature oocyte cultured in dbcAMP and FSH group had a higher rate of the embryos developed to the 8-cell stage (49.2%) than in the none treated or only dbcAMP treated group (26.5% and 27.6%). These results confirmed that the combination of dbcAMP 1mM and FSH 0.01 IU/ml could increase the quality of the mature oocytes and improved the preimplantation development of parthenogenetic diploid embryos

scholarly journals TWO ACTIONS OF CYCLIC AMP ON MELANOSOME MOVEMENT IN FROG SKIN

1973 ◽  
Vol 57 (3) ◽  
pp. 845-858 ◽  
Author(s):  
Bruce Magun
Keyword(s):  
Cyclic Amp ◽  
Frog Skin ◽  
Cytochalasin B ◽  
Motive Force ◽  
Dibutyryl Cyclic Amp ◽  
Hormonal Stimulation ◽  
Melanocyte Stimulating Hormone ◽  
Skin Lightening ◽  
Stimulating Hormone

Photomicrography and reflectance microphotometry were used to monitor melanosome movement in frog skin melanocytes in vitro in response to hormonal stimulation and cytochalasin B (CB). Melanocyte-stimulating hormone (MSH), theophylline, and dibutyryl cyclic AMP (DiBcAMP) induced melanosome dispersion (darkening) which was promptly arrested by cytochalasin B in concentrations of 5–20 µg/ml. Melanosome aggregation (skin lightening) occurred only after removal of the darkening agent (MSH, theophylline, or DiBcAMP) and proceeded in the presence or absence of CB. When CB was added to darkened skins, they did not lighten and melanosomes remained in the dispersed state. Use of CB has permitted the dissection of cyclic AMP-mediated melanosome dispersion into two distinct events. The first, induction of melanosome dispersion, is CB sensitive. The second action of intracellular cyclic AMP involves an uncoupling of the centripetal motive force, and is CB insensitive. In the latter process, production of cyclic AMP appears to produce the same result as application of microtubule-disrupting agents.

Dobutamine Antagonizes Epinephrine's Biochemical and Cardiotonic Effects 

1998 ◽  
Vol 89 (1) ◽  
pp. 49-57 ◽  
Author(s):  
Richard C. Prielipp ◽  
Drew A. MacGregor ◽  
Roger L. Royster ◽  
Neal D. Kon ◽  
Michael H. Hines ◽  
...  
Keyword(s):  
Artery Bypass ◽  
Phase 1 ◽  
Human Lymphocytes ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Camp Production ◽  
Isobolographic Analysis ◽  
Camp Generation ◽  
Vitro Model

Background Patients may receive more than one positive inotropic drug to improve myocardial function and cardiac output, with the assumption that the effects of two drugs are additive. The authors hypothesized that combinations of dobutamine and epinephrine would produce additive biochemical and hemodynamic effects. Methods The study was performed in two parts. Phase 1 used human lymphocytes in an in vitro model of cyclic adenosine monophosphate (cAMP) generation in response to dobutamine (10(-8) to 10(-4) M) or epinephrine (10(-9) M to 10(-5) M), and dobutamine and epinephrine together. Phase 2 was a clinical study in patients after aortocoronary artery bypass in which isobolographic analysis compared the cardiotonic effects of dobutamine (1.25, 2.5, or 5 microg x kg(-1) x min(-1)) or epinephrine (10, 20, or 40 ng x kg(-l) x min(-1)), alone or in combination. Results In phase 1, dobutamine increased cAMP production 41%, whereas epinephrine increased cAMP concentration approximately 200%. However, when epinephrine (10(-6) M) and dobutamine were combined, dobutamine reduced cAMP production at concentrations between 10(-6) to 10(-4) M (P = 0.001). In patients, 1.25 to 5 microg x kg(-1) x min(-1) dobutamine increased the cardiac index (CI) 15-28%. Epinephrine also increased the CI with each increase in dose. However, combining epinephrine with the two larger doses of dobutamine (2.5 and 5microg x kg(-1) x mi(-1)) did not increase the CI beyond that achieved with epinephrine and the lowest dose of dobutamine (1.25 microg x kg(-1) x min(-1)). In addition, the isobolographic analysis for equieffective concentrations of dobutamine and epinephrine suggests subadditive effects. Conclusions Dobutamine inhibits epinephrine-induced production of cAMP in human lymphocytes and appears to be subadditive by clinical and isobolographic analyses of the cardiotonic effects. These findings suggest that combinations of dobutamine and epinephrine may be less than additive.

scholarly journals The nucleoporin RanBP2 tethers the cAMP effector Epac1 and inhibits its catalytic activity

2011 ◽  
Vol 193 (6) ◽  
pp. 1009-1020 ◽  
Author(s):  
Martijn Gloerich ◽  
Marjolein J. Vliem ◽  
Esther Prummel ◽  
Lars A.T. Meijer ◽  
Marije G.A. Rensen ◽  
...  
Keyword(s):  
Catalytic Activity ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Negative Regulator ◽  
Camp Signaling ◽  
Nuclear Pore ◽  
Nucleotide Exchange ◽  
Nucleotide Exchange Factor ◽  
Wide Range

Cyclic adenosine monophosphate (cAMP) is a second messenger that relays a wide range of hormone responses. In this paper, we demonstrate that the nuclear pore component RanBP2 acts as a negative regulator of cAMP signaling through Epac1, a cAMP-regulated guanine nucleotide exchange factor for Rap. We show that Epac1 directly interacts with the zinc fingers (ZNFs) of RanBP2, tethering Epac1 to the nuclear pore complex (NPC). RanBP2 inhibits the catalytic activity of Epac1 in vitro by binding to its catalytic CDC25 homology domain. Accordingly, cellular depletion of RanBP2 releases Epac1 from the NPC and enhances cAMP-induced Rap activation and cell adhesion. Epac1 also is released upon phosphorylation of the ZNFs of RanBP2, demonstrating that the interaction can be regulated by posttranslational modification. These results reveal a novel mechanism of Epac1 regulation and elucidate an unexpected link between the NPC and cAMP signaling.

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