Adenosine 3′: 5′-Cyclic Monophosphate Response Elicited by Histamine and Adrenaline in Lungs of Normal and Allergic Guinea Pigs: Relationship of Histamine Release and Adenylate Cyclase Activity

1973 ◽  
Vol 1 (3) ◽  
pp. 720-722 ◽  
Author(s):  
J. WOHNLICH ◽  
F. RUFF ◽  
J. L. PARROT
Keyword(s):  
Adenylate Cyclase ◽  
Histamine Release ◽  
Guinea Pigs ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Cyclic Monophosphate ◽  
Relationship Of

Acetylcholine inhibits positive inotropic effect of cholera toxin in ventricular muscle

1982 ◽  
Vol 243 (3) ◽  
pp. H434-H441
Author(s):  
A. J. Pappano ◽  
P. M. Hartigan ◽  
M. D. Coutu
Keyword(s):  
Chick Embryo ◽  
Cyclic Amp ◽  
Adenylate Cyclase ◽  
Cholera Toxin ◽  
Positive Inotropic Effect ◽  
Phosphodiesterase Inhibitor ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Inotropic Effect ◽  
Cyclic Monophosphate

Acetylcholine (ACh, 10(-6) M) had no effect on basal adenylate cyclase activity (3.4 +/- 0.56 pmol cyclic AMP . min-1 . mg wet wt-1), adenosine 3',5'-cyclic monophosphate (cyclic AMP) content (0.88 +/- 0.09 pmol/mg wet wt), or the force of contraction in paced (2.5 Hz) chick embryo right ventricles superfused with Tyrode solution. After 60-180 min of superfusion in the presence of cholera toxin (5 x 10(-6) g/ml), adenylate cyclase activity (1.7 times), cyclic AMP content (2.4 times), and contractility (2.4 times) had increased significantly above basal levels. ACh reversed the positive inotropic effect of cholera toxin but did not change the increased activity of adenylate cyclase and content of cyclic AMP obtained in cholera toxin. Stimulation of adenylate cyclase by isoproterenol (ISO) was inhibited by ACh in the absence and presence of cholera toxin. ACh did not change guanosine 3',5'-cyclic monophosphate (cyclic GMP) content in the absence or presence of cholera toxin. Cholera toxin has actions on chick embryo ventricle similar to those of the beta-adrenergic agonist, ISO, and the phosphodiesterase inhibitor, isobutylmethylxanthine. The ability of ACh to reverse the positive inotropic effect of cholera toxin without preventing the accumulation of cyclic AMP may involve the prevention or reversal of cyclic AMP-dependent phosphorylation. In this regard, reduction of Ca2+ influx through voltage-sensitive membrane channels may be an essential component of muscarinic inhibition.

The Relationship of Growth and Adenylate Cyclase Activity in Cultured Thyroid Cells: Separate Bioeffects of Thyrotropin

Endocrinology ◽  
1983 ◽  
Vol 112 (1) ◽  
pp. 71-79 ◽  
Author(s):  
WILLIAM A. VALENTE ◽  
PAOLO VITTI ◽  
LEONARD D. KOHN ◽  
MARIA L. BRANDI ◽  
CARLO M. ROTELLA ◽  
...  
Keyword(s):  
Adenylate Cyclase ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Thyroid Cells ◽  
Relationship Of ◽  
The Relationship

Adenosine receptor-mediated coronary artery relaxation and cyclic nucleotide production

1991 ◽  
Vol 261 (2) ◽  
pp. H343-H348 ◽  
Author(s):  
D. J. Cushing ◽  
G. L. Brown ◽  
M. H. Sabouni ◽  
S. J. Mustafa
Keyword(s):  
Coronary Artery ◽  
Adenylate Cyclase ◽  
Adenosine Receptor ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Cyclic Monophosphate ◽  
Cgs 21680 ◽  
Free Membrane

We investigated the involvement of adenosine 3',5'-cyclic monophosphate (cAMP) and guanosine 3',5'-cyclic monophosphate (cGMP) in adenosine (ADO) receptor-mediated coronary artery relaxation. Rings from left anterior descending coronary artery, with the endothelium mechanically removed, contracted with prostaglandin F2 alpha and relaxed in a concentration-dependent manner to ADO, 2-chloroadenosine (CAD), l-N6-(2-phenylisopropyl)adenosine (R-PIA), and 5'-(N-ethylcarboxamido)adenosine (NECA). These relaxations were blocked by addition of the ADO receptor antagonist 8-(sulfophenyl)theophylline (8-SPT), indicating ADO receptor involvement. In an endothelium-free membrane preparation, ADO, CAD, and R-PIA all stimulated adenylate cyclase activity in a concentration-dependent manner, and these responses were blocked by 8-SPT. The increase in adenylate cyclase activity produced by ADO, CAD, and R-PIA was completely dependent on the presence of guanosine 5'-triphosphate, suggesting G protein involvement. Surprisingly, NECA and CGS-21680 did not increase adenylate cyclase activity. Unlike atrial natriuretic factor, neither NECA, CAD, R-PIA, nor ADO increased guanylate cyclase activity, suggesting that cGMP is not involved in ADO receptor-mediated relaxation. Data presented in this study support the hypothesis that ADO receptor-mediated coronary artery relaxation may involve cAMP; however, the inability of NECA and CGS-21680 to stimulate adenylate cyclase suggests that the ADO receptor-signaling mechanisms in coronary artery may be more complicated than agonist interaction with a single adenylate cyclase-coupled A2 adenosine receptor.

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