Urinary Adenosine 3’,5′-Cyclic Monophosphate: Effects of Electroconvulsive Therapy

1976 ◽  
Vol 129 (2) ◽  
pp. 173-177 ◽  
Author(s):  
Richard B. Moyes ◽  
Isabel C. A. Moyes
Keyword(s):  
Cyclic Amp ◽  
Electroconvulsive Therapy ◽  
Consistent Pattern ◽  
Cyclic Monophosphate ◽  
Urinary Cyclic Amp

SummarySerial studies of urinary cyclic AMP in in-patients undergoing electroconvulsive therapy (ECT) have been carried out. No consistent pattern of change following ECT could be demonstrated. The results do not support earlier reports of large rises in urinary cAMP directly after administration of ECT.

Urinary Cyclic AMP in ‘Endogenous' and ‘Neurotic’ Depression

1975 ◽  
Vol 126 (1) ◽  
pp. 49-55 ◽  
Author(s):  
K. Sinanan ◽  
A. M. B. Keatinge ◽  
P. G. S. Beckett ◽  
W. Clayton Love
Keyword(s):  
Cyclic Amp ◽  
Second Messenger ◽  
Adenyl Cyclase ◽  
Induced Responses ◽  
High Concentration ◽  
Cyclic Monophosphate ◽  
Cyclic Amp Phosphodiesterase ◽  
Urinary Cyclic Amp ◽  
The Brain

Since the discovery of adenosine 3'5'-cyclic monophosphate (cyclic AMP) by Sutherland and Rall (1958), the concept has evolved that this nucleotide acts as the second messenger substance for many neurotransmitter and hormone-induced responses (Sutherland, Robison and Butcher, 1968). Cyclic AMP occurs in high concentration in the brain. Cyclic AMP is functionally closely related, and possibly fundamental, to the action of catecholamines and serotonin, both of which have been implicated in the amine hypothesis of depression (Granville-Grossman, 1971). Cyclic AMP is formed from ATP by the action of an enzyme adenyl cyclase, and it is degraded by the enzyme cyclic-AMP-phosphodiesterase (Lancet, Editorial, 1970) both of which occur in brain.

Urinary Excretion of Adenosine 3’: 5′-Cyclic Monophosphate in Depressive Illness

1974 ◽  
Vol 125 (586) ◽  
pp. 275-279 ◽  
Author(s):  
Graham J. Naylor ◽  
David A. Stansfield ◽  
Susan F. Whyte ◽  
Frederick Hutchinson
Keyword(s):  
Cyclic Amp ◽  
Urinary Excretion ◽  
Affective State ◽  
Depressive Illness ◽  
Control Group ◽  
Cyclic Monophosphate ◽  
Manic Depressive ◽  
Two Samples ◽  
Urinary Cyclic Amp ◽  
Depressive Patients

Changes in the excretion of adenosine 3’:5′-cyclic monophosphate (cyclic AMP) have been reported in depressive illness. Abdulla and Hamadah (1970) reported that urinary cyclic AMP excretion was lower than normal during depression and increased with recovery. However, these results were based on single 24-hour urine collections during depression and on recovery, with no creatinine estimations to suggest that the collections were complete. There was no control of diet, drugs or activity. The controls do not appear to have been matched for age. Paul, Ditzion, Pauk and Janowsky (1970) reported that the cyclic AMP excretion in neurotic depression was higher and in psychotic depression was lower than in a control group, but neither difference was statistically significant. However, on enlarging the study by including more psychotic depressives they reported that the cyclic AMP excretion of this group was significantly less than that of the controls (Paul, Cramer and Goodwin, 1971). These workers had controlled the patients' drug and dietary (but not fluid) intake. There appeared to be only minimal control of activity. The results were based on approximately two samples of urine per subject, which were very carefully checked for completeness of collection. Unfortunately the age of the controls (19–22 years) was very different from that of the patients (25–64 years). On two small groups of patients treated with either Laevodopa or lithium carbonate, they reported that changes in affective state were accompanied by changes in the urinary excretion of cyclic AMP. However, in serial studies on manic-depressive patients Paul, Cramer and Bunney (1971) failed to show a correlation between mood rating and cyclic AMP excretion in five out of seven patients; but they reported that the cyclic AMP excretion was increased on the day of rapid switch from depression to mania. The above groups of workers had used an enzymatic-isotope displacement technique to estimate the cyclic AMP. Brown, Salway, Albano, Hullin and Ekins (1972), using a saturation method to assay cyclic AMP, found no correlation between mood and cyclic AMP excretion in two short-cycle manic-depressive patients. Jenner, Sampson, Thompson, Somerville, Beard and Smith (1972) wrote: ‘We have measured daily excretion by a number of depressed and manic depressive patients over periods covering several mood changes without being able to establish any consistent correlation between cyclic AMP excretion and mood, … However, in one unusual case we have found a very marked correlation‘. We (Naylor, Dick, Dick, Moody and Stansfield, 1974) were unable to demonstrate any relationship between urinary cyclic AMP excretion and mood in a patient with recurrent psychotic episodes, in which depressive features predominated.

scholarly journals Intracellular calcium and adenosine 3′,5′-cyclic monophosphate as mediators of potassium-induced aldosterone secretion

1985 ◽  
Vol 228 (1) ◽  
pp. 69-76 ◽  
Author(s):  
I Kojima ◽  
K Kojima ◽  
H Rasmussen
Keyword(s):  
Arachidonic Acid ◽  
Cyclic Amp ◽  
Intracellular Calcium ◽  
Secretory Response ◽  
Ionophore A23187 ◽  
Small Decrease ◽  
Aldosterone Secretion ◽  
Cyclic Monophosphate ◽  
A Value ◽  
Glomerulosa Cells

We compared the action of K+ on aldosterone secretion from isolated bovine adrenal glomerulosa cells with that of ionophore A23187. Addition of either 50 nM-A23187 or 8 mM-K+ to perifused cells induces a similar initial aldosterone-secretory responses, and a similar sustained increases in Ca2+ entry. However, K+-induced secretion is more sustained than is A23187-induced secretion, even though each agonist appears to act by increasing Ca2+ entry into the cells. When [3H]inositol-labelled cells are stimulated by 8 mM-K+, a small decrease in phosphatidylinositol 4,5-bisphosphate [PtdIns(4,5)P2] is observed. This decrease is not accompanied by an increase in inositol trisphosphate (InsP3) concentration. Also, if [3H]arachidonic acid-labelled cells are exposed to 8 mM-K+, there is no increase in [3H]diacylglycerol production. When [3H]inositol-labelled cells are stimulated by 50 nM-A23187, a small decrease in PtdIns(4,5)P2 is observed. This decrease is not accompanied by an increase in InsP3. The cyclic AMP content of K+-treated cells was approximately twice that in A23187-treated cells. If cells are perifused simultaneously with 50 nM-forskolin and 50 nM-A23187, the initial aldosterone-secretory response is similar to that induced by A23187 alone, and the response is sustained rather than transient, and is similar to that seen during perifusion of cells with 8 mM-K+. This dose of forskolin (50 nM) causes an elevation of cyclic AMP concentration in A23187-treated cells, to a value similar to that in K+-treated cells. These results indicate that, in K+-treated cells, a rise in cyclic AMP content serves as a positive sensitivity modulator of the Ca2+ message, and plays a key role in mediating the sustained aldosterone-secretory response.

Mannose utilization in Escherichia coli requires cyclic AMP but not an exogenous inducer

1980 ◽  
Vol 26 (12) ◽  
pp. 1508-1511 ◽  
Author(s):  
Ann D. E. Fraser ◽  
Hiroshi Yamazaki
Keyword(s):  
Escherichia Coli ◽  
Carbon Source ◽  
Cyclic Amp ◽  
Adenylyl Cyclase ◽  
Sole Carbon Source ◽  
Receptor Protein ◽  
Deficient Mutant ◽  
Phosphotransferase System ◽  
Cyclic Amp Receptor Protein ◽  
Cyclic Monophosphate

It has not been clarified whether the utilization of mannose by Escherichia coli requires adenosine 3′,5′-cyclic monophosphate (cyclic AMP). Using an adenylyl cyclase deficient mutant (CA8306B) and a cyclic AMP receptor protein (CRP) deficient mutant (5333B) we have shown that the utilization of mannose is dependent on the cyclic AMP–CRP complex. 2-Deoxyglucose (DG) is a nonmetabolizable glucose analog specific for the phosphotransferase system (PTS) which transports mannose (termed here PTSM). Growth of CA8306B on glycerol is unaffected by addition of the analog, whereas growth of the strain on glycerol plus cyclic AMP ceases im mediately upon addition of DG. These results suggest that the formation of PTSM is dependent on cyclic AMP. In addition, CA8306B grown on glycerol plus cyclic AMP can immediately utilize mannose when transferred to a medium containing mannose as a sole carbon source, whereas the same strain grown on glycerol without cyclic AMP cannot utilize mannose when so transferred. These results suggest that the formation of PTSM does not require an exogenous inducer.

Urinary cyclic AMP excretion is increased inMacaca fascicularis andMacaca mulatta compared to humans

1991 ◽  
Vol 23 (3) ◽  
pp. 201-206
Author(s):  
John L. Stock ◽  
James A. Coderre ◽  
James A. Simon
Keyword(s):  
Cyclic Amp ◽  
Urinary Cyclic Amp

Dissociation between plasma, urine, and renal papillary cyclic AMP content following vasopressin and DDAVP

1979 ◽  
Vol 237 (3) ◽  
pp. F218-F225 ◽  
Author(s):  
M. J. Bia ◽  
S. Dewitt ◽  
J. N. Forrest
Keyword(s):  
Cyclic Amp ◽  
Urine Osmolality ◽  
Brattleboro Rats ◽  
Renal Papilla ◽  
Brattleboro Rat ◽  
Clearance Studies ◽  
Urinary Cyclic Amp ◽  
Stimulation Of

The effects of in vivo physiologic doses of vasopressin and 1-deamino-8-D-arginine vasopressin (DDAVP) on the cyclic AMP content of plasma, urine, and renal papillary tissue were determined in the ADH-deficient Brattleboro rat. During clearance studies, plasma cyclic AMP concentrations and both total and nephrogenous urinary cyclic AMP excretion in vasopressin- and DDAVP-treated rats were similar to the values in time-matched controls. In contrast, in situ renal papillary cyclic AMP content was higher (P less than 0.001) in both vasopressin- (35.7 +/- 3.6 pmol/mg protein) and DDAVP- (29.7 +/- 2.2 pmol/mg protein) treated rats compared to controls (15.1 +/- 1.3 pmol/mg protein). Endogenous stimulation of vasopressin by dehydration in normal rats increased both papillary cyclic AMP content (27.1 +/- 2.7 pmol/mg protein) and urine osmolality, whereas no change in papillary cyclic AMP was observed following dehydration in Brattleboro rats (13.6 +/- 0.8 pmol/mg protein) despite an increase in urine osmolality. The results demonstrate that changes in cyclic AMP following in vivo vasopressin are best demonstrated by measurement of in situ cyclic AMP content of the renal papilla, whereas total urinary cyclic AMP and nephrogenous cyclic AMP are not useful indices of tubular sensitivity to this hormone.

Urinary Cyclic Amp Excretion in Thyroid Disease

1974 ◽  
Vol 47 (5) ◽  
pp. 19P-20P
Author(s):  
D. J. Carter ◽  
D. A. Heath ◽  
R. Hoffenberg
Keyword(s):  
Cyclic Amp ◽  
Thyroid Disease ◽  
Urinary Cyclic Amp
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