Effect of 1,25-dihydroxycholecalciferol on adenosine 3′,5′-cyclic monophosphate production in calvaria of mice

1978 ◽  
Vol 25 (1) ◽  
pp. 223-225 ◽  
Author(s):  
U. Gebauer ◽  
H. Fleisch
Keyword(s):  
Cyclic Monophosphate

Hydrolysis and methanolysis of the phenyl ester of thymidine 3',5'-cyclic monophosphate: pH-dependent competition between PO and CO bond ruptures

1996 ◽  
Vol 61 (s1) ◽  
pp. 26-29
Author(s):  
Mikko Oivanen ◽  
Jaana Varila ◽  
Teemu Hankamaki ◽  
Leo H. Koole ◽  
Harri Lönnberg
Keyword(s):  
Phenyl Ester ◽  
Cyclic Monophosphate ◽  
Ph Dependent

Glycogenolytic rates and cAMP in livers of rats running at different treadmill speeds

1983 ◽  
Vol 245 (3) ◽  
pp. R353-R356
Author(s):  
W. W. Winder ◽  
M. A. Beattie ◽  
E. O. Fuller
Keyword(s):  
Liver Glycogen ◽  
Work Rate ◽  
Curvilinear Relationship ◽  
Camp Concentration ◽  
Running Speed ◽  
Cyclic Monophosphate ◽  
High Degree ◽  
The Relationship ◽  
Camp Levels ◽  
Liver Glycogenolysis

The purposes of this study were to determine the effect of different work rates on the rate of liver glycogenolysis and to determine the relationship between liver adenosine 3',5'-cyclic monophosphate (cAMP) levels and the glycogenolytic rate. Rats were run at treadmill speeds ranging from 10 to 34 m/min up a 15% grade for either 30 or 60 min. Both the magnitude of the decrease in liver glycogen and the increase in hepatic cAMP were dependent on the running speed and the duration of running. At the highest work rate a disproportionate acceleration in the liver glycogenolytic rate was observed compared with that at lower work loads, thus resulting in a curvilinear relationship between work rate and liver glycogenolytic rate. A high degree of correlation was found between the liver glycogenolytic rate and hepatic cAMP concentration (r = 0.98). This observation is consistent with the idea that hepatic glycogenolytic rates are determined by cAMP-mediated mechanisms.

Biochemical activities of tubercidin 3', 5'-cyclic monophosphate in rat epididymal adipose tissue

1971 ◽  
Vol 20 (1) ◽  
pp. 249-251 ◽  
Author(s):  
Melvin Blecher ◽  
J.T. Ro'ane ◽  
P.D. Flynn
Keyword(s):  
Adipose Tissue ◽  
Epididymal Adipose Tissue ◽  
Cyclic Monophosphate

Enhanced role of K+ channels in relaxations of hypercholesterolemic rabbit carotid artery to NO

1995 ◽  
Vol 269 (3) ◽  
pp. H805-H811 ◽  
Author(s):  
S. Najibi ◽  
R. A. Cohen
Keyword(s):  
Carotid Artery ◽  
Sodium Nitroprusside ◽  
Channel Blocker ◽  
Isometric Tension ◽  
K Channel ◽  
K Channels ◽  
Rabbit Carotid Artery ◽  
Cyclic Monophosphate ◽  
Endothelium Dependent Relaxation

Endothelium-dependent relaxations to acetylcholine remain normal in the carotid artery of hypercholesterolemic rabbits, but unlike endothelium-dependent relaxations of normal rabbits, they are inhibited by charybdotoxin, a specific blocker of Ca(2+)-dependent K+ channels. Because nitric oxide (NO) is the mediator of endothelium-dependent relaxation and can activate Ca(2+)-dependent K+ channels directly or via guanosine 3',5'-cyclic monophosphate, the present study investigated the role of Ca(2+)-dependent K+ channels in relaxations caused by NO, sodium nitroprusside, and 8-bromoguanosine 3',5'-cyclic monophosphate (8-Brc-GMP) in hypercholesterolemic rabbit carotid artery. Isometric tension was measured in rabbit carotid artery denuded of endothelium from normal and hypercholesterolemic rabbits which were fed 0.5% cholesterol for 12 wk. Under control conditions, relaxations to all agents were similar in normal and hypercholesterolemic rabbit arteries. Charybdotoxin had no significant effect on relaxations of normal arteries to NO, sodium nitroprusside, or 8-BrcGMP, but the Ca(2+)-dependent K+ channel blocker significantly inhibited the relaxations caused by each of these agents in the arteries from hypercholesterolemic rabbits. By contrast, relaxations to the calcium channel blocker nifedipine were potentiated to a similar extent by charybdotoxin in both groups. In addition, arteries from hypercholesterolemic rabbits relaxed less than normal to sodium nitroprusside when contracted with depolarizing potassium solution. These results indicate that although nitrovasodilator relaxations are normal in the hypercholesterolemic rabbit carotid artery, they are mediated differently, and to a greater extent, by Ca(2+)-dependent K+ channels. These data also suggest that K+ channel-independent mechanism(s) are impaired in hypercholesterolemia.

Glucocorticoid regulation of epithelial sodium channel genes in human fetal lung

1997 ◽  
Vol 273 (1) ◽  
pp. L227-L233 ◽  
Author(s):  
V. C. Venkatesh ◽  
H. D. Katzberg
Keyword(s):  
Rna Polymerase Ii ◽  
Actinomycin D ◽  
Critical Role ◽  
Fetal Lung ◽  
Explant Culture ◽  
Late Gestation ◽  
Na Channel ◽  
Second Trimester ◽  
Cyclic Monophosphate ◽  
Human Fetal Lung

Pulmonary epithelial Na+ channels (ENaC), composed of three distinct subunits (alpha, beta, and gamma), play a critical role in the regulation of fluid reabsorption from airspaces of late-gestation fetal lung. We studied the expression of ENaC subunit genes in cultured human fetal lung. All three mRNAs were expressed at low levels in second trimester lung (13-32% of adult values at 24 wk gestation). There was a spontaneous increase of approximately threefold over preculture values of all three subunits within 24 h of explant culture in serum-free Waymouth's medium. Dexamethasone (Dex) induced all three mRNAs by two- to threefold. Maximal induction was noted by 8 h with 30-100 nM Dex and half-maximal stimulation with 3-10 nM Dex. Cycloheximide decreased basal expression of all three subunits by 8 h but did not alter the response to Dex. Actinomycin D and 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole (DRB), inhibitors of RNA polymerase II, decreased the basal and the Dex-induced expression of all three subunits with a more marked effect on human hENaC-gamma than on hENaC-alpha or hENaC-beta. Under conditions where transcription was blocked by actinomycin D or DRB, Dex did not alter the stability of the three mRNAs. Triiodothyronine (T3) at low (2 nM) or high (100 nM) concentrations had no effect on the expression of the three subunits in the presence or absence of low (10 nM) or high (100 nM) concentrations of Dex for 8 or 24 h. Similarly, 8-bromoadenosine 3',5'-cyclic monophosphate (2 microM) had no effect on basal or Dex-induced increase in the three subunits. We conclude that the three Na+ channel subunit genes are expressed in second trimester human fetal lung and are coordinately upregulated by glucocorticoid hormones but not by T3 or adenosine 3',5'-cyclic monophosphate. Glucocorticoid induction is receptor mediated, is primarily transcriptional, and does not require the induction of an intermediate protein for transcriptional enhancement. We speculate that induction of lung ENaC may contribute to the beneficial effects of antenatal glucocorticoids in premature babies.

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