Cyclic AMP-Dependent and -Independent Effects of β-Adrenergic Stimulation on the Contraction—Relaxation Cycle of Spontaneously Beating Rat Atria

1982 ◽  
pp. 47-57
Author(s):  
T. Metsä-Ketelä
Keyword(s):  
Cyclic Amp ◽  
Adrenergic Stimulation ◽  
Relaxation Cycle ◽  
Rat Atria ◽  
Independent Effects

Papaverine-induced positive inotropism with failure to increase cyclic AMP in rat atria

1986 ◽  
Vol 131 (1) ◽  
pp. 141-144
Author(s):  
Pedro Aramendía ◽  
Claudio D. Eisenschlos ◽  
María T. Márquez
Keyword(s):  
Cyclic Amp ◽  
Rat Atria ◽  
Positive Inotropism

STIMULATION BY β2-ADRENERGIC RECEPTORS OF THE PRODUCTION OF CYCLIC AMP AND PROGESTERONE IN RAT OVARIAN TISSUE

1980 ◽  
Vol 87 (1) ◽  
pp. 123-129 ◽  
Author(s):  
ALBERT RATNER ◽  
G. K. WEISS ◽  
CAROLYN R. SANBORN
Keyword(s):  
Cyclic Amp ◽  
Adrenergic Receptors ◽  
Ovarian Tissue ◽  
Chorionic Gonadotrophin ◽  
Human Chorionic Gonadotrophin ◽  
Adrenergic Stimulation ◽  
Immature Rats ◽  
Luteal Tissue ◽  
Pregnant Mare Serum Gonadotrophin ◽  
Stimulation Of

Ovarian tissue from immature rats treated with pregnant mare serum gonadotrophin (PMSG) or PMSG and human chorionic gonadotrophin was incubated in Medium 199. Stimulation of the formation of cyclic AMP in follicular and luteal tissue by terbutaline (10−5 mol/l), a selective β2-agonist, was blocked by butoxamine (10−5 mol/l), a selective β2-antagonist, whereas practolol (10−5 mol/l), a selective β1-antagonist, was ineffective. Propranolol (10−5 mol/l), a non-selective β-antagonist, butoxamine nor practolol affected the increase in cyclic AMP promoted by the addition of 1 μg LH. Stimulation of the production of progesterone in both follicular and luteal tissue by terbutaline was blocked by butoxamine, but not by practolol. These findings indicated that β-adrenergic stimulation of ovarian cyclic AMP and progesterone is mediated by β2-adrenergic receptors.

Sources of Human Plasma Cyclic AMP. Examinations before and after Beta2 Adrenergic Stimulation

1981 ◽  
Vol 9 (6) ◽  
pp. 521-525 ◽  
Author(s):  
Peter Endres ◽  
Christine Klock ◽  
Rolf Günther
Keyword(s):  
Cyclic Amp ◽  
Inferior Vena Cava ◽  
Right Ventricle ◽  
Subcutaneous Injection ◽  
Inferior Vena ◽  
Vena Cava ◽  
Adrenergic Stimulation ◽  
Arterial Blood ◽  
Before And After ◽  
General Influence

Plasma cyclic AMP was measured in different vessels in seventeen volunteers before and after stimulation with terbutaline. Differences between arterial blood and blood from the hepatic vein, right ventricle, inferior vena cava and a cubital vein could not be demonstrated. Only in the renal vein was the concentration of cyclic AMP decreased. Our results indicate that cyclic AMP is not generated from any specific isolated organ and that changes in cyclic AMP after subcutaneous injection of terbutaline reflect a general influence of this drug.

Cyclic AMP Second-Messenger Signal Amplification in Depression

1988 ◽  
Vol 152 (5) ◽  
pp. 665-669 ◽  
Author(s):  
Richard P. Ebstein ◽  
Bernard Lerer ◽  
Baruch Shapira ◽  
Zecharia Shemesh ◽  
Daniel G. Moscovich ◽  
...  
Keyword(s):  
Cyclic Amp ◽  
Signal Amplification ◽  
Antidepressant Treatment ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Late Night ◽  
Depressed Patients ◽  
Cyclic Amp Accumulation ◽  
Significant Clinical Improvement ◽  
Age And Sex

Beta-adrenergic-mediated cyclic AMP accumulation was reduced in lymphocytes obtained from depressed patients from that observed in an age- and sex-matched group of control subjects. Among the depressed patients, those not responding to treatment showed significantly lower pretreatment responses to isoproterenol compared with patients who exhibited significant clinical improvement during antidepressant treatment. Late-night (terminal) insomnia was significantly associated with the blunted response to beta-adrenergic stimulation. In depressed patients with the lowest isoproterenol response, the effect of forskolin (which acts distal to the receptor and directly stimulates the catalytic subunit) on cyclic AMP accumulation was also significantly decreased. This suggests that post-receptor modulations of signal amplification also play a role in the reduced response to beta-adrenergic stimulation in depression.

Isoproterenol exerts cyclic AMP independent effects on DNA synthesis in cultured adventitial fibroblasts from spontaneously hypertensive and Wistar–Kyoto rats

1994 ◽  
Vol 72 (10) ◽  
pp. 1208-1214 ◽  
Author(s):  
Shannon L. Venance ◽  
Brian M. Bennett ◽  
Stephen C. Pang
Keyword(s):  
Growth Factor ◽  
Cyclic Amp ◽  
Dna Synthesis ◽  
Spontaneously Hypertensive Rat ◽  
Signal Transduction Pathway ◽  
Spontaneously Hypertensive ◽  
Adventitial Fibroblasts ◽  
Wistar Kyoto ◽  
Independent Effects

Understanding the mechanism behind the growth response evident in the vasculature of the spontaneously hypertensive rat (SHR) remains elusive. Fibroblasts from the aortic adventitial layer of the SHR manifest the heightened proliferative rate in vitro relative to Wistar–Kyoto (WKY) rats that is conspicuous in cultured aortic smooth muscle cells. The adenylyl-cyclase/cyclic AMP signal transduction pathway is believed to be altered in hypertensive people and animals such that responses to β-adrenoceptor activation are blunted. The present study examined the effects of β-adrenoceptor-mediated versus direct activation of adenylylcyclase on intracellular cyclic AMP accumulation and subsequent DNA synthesis in cultured aortic fibroblasts. We hypothesized that elevation of cyclic AMP levels by both isoproterenol and forskolin would normalize the proliferative capacity of SHR fibroblasts. Forskolin increased intracellular cyclic AMP levels and inhibited epidermal growth factor stimulated thymidine incorporation in an equivalent manner in both SHR and WKY adventitial fibroblasts, implying that there is no difference in adenylylcyclase activity. Isoproterenol elevated cyclic AMP levels to a significantly greater degree in the SHR than did forskolin, and yet, relative to forskolin, attenuated growth factor induced DNA synthesis to a lesser extent. These data suggest that isoproterenol, via β-adrenoceptor activation, exhibits both cyclic AMP dependent and cyclic AMP independent effects in adventitial fibroblasts. The cyclic AMP independent effects of isoproterenol oppose the expected observations due to cyclic AMP and may offer an explanation to the blunted responses to β-adrenoceptor activation evident both in vitro and in vivo.Key words: spontaneously hypertensive rats, cultured adventitial fibroblasts, aorta, isoproterenol, forskolin, DNA synthesis, cyclic AMP.

Effects of isoproterenol on cylic-AMP metabolism in rat ventral prostate

1976 ◽  
Vol 54 (3) ◽  
pp. 327-335 ◽  
Author(s):  
B. K. Tsang ◽  
R. L. Singhal
Keyword(s):  
Protein Kinase ◽  
Cyclic Amp ◽  
Adenylate Cyclase ◽  
Kinase Activity ◽  
Activity Ratio ◽  
Ventral Prostate ◽  
Adrenergic Stimulation ◽  
Dependent Protein Kinase ◽  
Dependent Protein ◽  
Stimulation Of

β-Adrenergic stimulation of the ventral prostate cyclic-AMP system was investigated by examining the influence of isoproterenol on endogenous cyclic-AMP levels as well as on the activities of adenylate cyclase (EC 4.6.1.1) and cyclic-AMP-dependent and independent protein kinases (EC 2.7.1.37). Administration of isoproterenol (1 mg/kg, ip) resulted in rapid elevation of adenylate cyclase activity (119%) and cyclic-AMP levels (593%). The observed isoproterenol-stimulated changes in cyclic-AMP metabolism of the ventral prostate were time-dependent and maximal stimulation was seen 5 min after treatment with this β-adrenergic agonist. The increases in prostatic adenylate cyclase and cyclic-AMP also were related to the dose of isoproterenol administered and maximal enhancement of these parameters was seen with 1 mg/kg dose of the agonist. Whereas pretreatment of rats with propranolol (3 mg/kg, ip) partially reversed these alterations, administration of an α-adrenergic antagonist, phentolamine, even at a dose of 5 mg/kg, failed to elicit any appreciable effect. Stimulation of prostatic soluble protein kinase by isoproterenol was associated with a decrease (33%) in the activity of the cyclic-AMP-dependent protein kinase with a concomitant increase (25%) in that of the independent enzyme. Whereas the ability of the enzyme to bind cyclic-[3H] AMP in vitro was decreased (54%) following isoproterenol treatment, the protein kinase activity ratio (−cyclic-AMP/+cyclic-AMP) was significantly elevated from 0.51 ± 0.05 to 0.95 ± 0.08. Although propranolol alone had little or no effect on these parameters, it inhibited partially the isoproterenol-induced alterations in cyclic-AMP-dependent protein kinase and the cyclic-AMP binding capacity. Treatment with propranolol also blocked the increases in the kinase activity ratio and in the activity of cyclic-AMP-independent enzyme seen with isoproterenol. Data suggest that the concentration of ventral prostate cyclic-AMP as well as the activities of adenylate cyclase and cyclic-AMP-dependent and independent form of protein kinases are subject to modulation by β-adrenergic stimulation.

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