Computer simulations of the rate of change of concentration of adenosine 3′:5′-cyclic monophosphate after stimulation of adenylate cyclase activity

1980 ◽  
Vol 8 (1) ◽  
pp. 139-140
Author(s):  
DAVID A. FELL
Keyword(s):  
Adenylate Cyclase ◽  
Computer Simulations ◽  
Rate Of Change ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Cyclic Monophosphate ◽  
Stimulation Of

Stimulation of Thyroid Adenylate Cyclase Activity in Sera of Patients with Nonthyroidal Illness

1986 ◽  
pp. 385-389
Author(s):  
F. Kakezono ◽  
S. Yamashita ◽  
N. Yokoyama ◽  
S. Morita ◽  
S. Okamoto ◽  
...  
Keyword(s):  
Adenylate Cyclase ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Nonthyroidal Illness ◽  
Stimulation Of

Prostaglandin E2-binding sites and cAMP production in porcine fundic mucosa

1981 ◽  
Vol 241 (4) ◽  
pp. G313-G320
Author(s):  
B. L. Tepperman ◽  
B. D. Soper
Keyword(s):  
Adenylate Cyclase ◽  
Prostaglandin E2 ◽  
Binding Site ◽  
Binding Sites ◽  
Biologically Active ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Scatchard Analysis ◽  
Fundic Mucosa ◽  
Stimulation Of

Biologically active [3H]prostaglandin E2 (PGE2) bound rapidly and specifically to membrane fractions from hog fundic mucosa. Optimal binding occurred in the 30,000-g membrane preparation at 37 degrees C (pH 5.0). Scatchard analysis of specific PgE2 binding revealed the presence of a heterogeneous population of binding sites with Kd values and binding site concentrations of approximately 1 X 10(-9) M and 1 fmol/mg prot and 2 X 10(-8) M and 20 fmol/mg prot, respectively. Specific binding was inhibited by the following agents in descending order of potency: PGE1, PGA2, PGD2, 6-keto-PGF1 alpha, and thromboxane B2. Trypsin treatment or boiling reduced or abolished specific PGE2 binding. PGE2 stimulated cAMP formation in the 2,500-g fraction, with an approximate Km of 1 X 10(-6) M, but stimulation of adenylate cyclase activity by PG was not evident in the 16,000-g or 30,000-g tissue preparations. These results suggest that a specific PGE2-binding site exists in the 16,000-g and 30,000-g fractions of porcine fundic mucosa, although an increase in cAMP-forming capacity could not b of 1 X 10(-6) M, but stimulation of adenylate cyclase activity by PG was not evident in the 16,000-g or 30,000-g tissue preparations. These results suggest that a specific PGE2-binding site exists in the 16,000-g and 30,000-g fractions of porcine fundic mucosa, although an increase in cAMP-forming capacity could not b of 1 X 10(-6) M, but stimulation of adenylate cyclase activity by PG was not evident in the 16,000-g or 30,000-g tissue preparations. These results suggest that a specific PGE2-binding site exists in the 16,000-g and 30,000-g fractions of porcine fundic mucosa, although an increase in cAMP-forming capacity could not be localized in these fractions in vitro.

Effect of histamine on canine gastric mucosal adenylate cyclase.

1977 ◽  
Vol 232 (1) ◽  
pp. E35
Author(s):  
R R Dozois ◽  
A Wollin ◽  
R D Rettmann ◽  
T P Dousa
Keyword(s):  
Gastric Mucosa ◽  
Cyclic Amp ◽  
Adenylate Cyclase ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Antral Mucosa ◽  
Fundic Mucosa ◽  
H2 Receptors ◽  
Dose Dependent ◽  
Stimulation Of

The effects of histamine, Nalpha-dimethylhistamine, 4,5-methylhistamine, Ntau-methylhistamine, pentagastrin, carbachol, and NaF on the adenylate cyclase activity from canine gastric mucosa were investigated in cell-free preparations. In gastric fundic mucosa, histamine (10(-4) M), Nalpha-dimethylhistamine (10(-4) M), 4,5-methylhistamine (10(-4 M), and NaF (10)-2) M) significantly (P less than 0.001) increased adenylate cyclase activity (means+/-SE) by 44.7+/-6.6, 49.4+/-6.7, 34.0+/-6.4, and 572.0+/-100%, respectively, above basal activity. The effect of histamine and Na-dimethyl histamine was dose-dependent. In contrast, other tested agents failed to stimulate the formation of cyclic AMP in gastric fundic mucosa. Metiamide (10(-4) M) blocked the stimulation of fundic mucosa adenylate cyclase by histamine and Nalpha-dimethylhistamine, without significantly altering basal and NaF-induced adenylate cyclase activity. Histamine, however, did not stimulate the adenylate cyclase activity from the gastric antral mucosa. The findings support the proposal that the canine gastric acid response to histamine may be mediated by cyclic AMP formed in response to stimulation of histamine H2-receptors.

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