In vitro Activation of rat gastric mucosal adenylate cyclase by tetragastrin

1981 ◽  
Vol 91 (4) ◽  
pp. 474-476
Author(s):  
A. A. Karelin ◽  
L. M. Petukhova
Keyword(s):  
Adenylate Cyclase ◽  
In Vitro Activation

scholarly journals In Vitro Activation of Adenylate Cyclase of Atrophic Celiac Intestinal Mucosa by Wheat Gliadin-Derived Peptides

1986 ◽  
Vol 20 (1) ◽  
pp. 42-44 ◽  
Author(s):  
L Beguinot ◽  
S Auricchio ◽  
J E Bernardin ◽  
G De Ritis ◽  
M De Vincenzi ◽  
...  
Keyword(s):  
Adenylate Cyclase ◽  
Intestinal Mucosa ◽  
In Vitro Activation ◽  
Wheat Gliadin

scholarly journals In vitro activation of CMV-specific human CD8+ T cells by adenylate cyclase toxoids delivering pp65 epitopes

2011 ◽  
Vol 47 (2) ◽  
pp. 243-250 ◽  
Author(s):  
J Jelinek ◽  
I Adkins ◽  
Z Mikulkova ◽  
J Jagosova ◽  
R Pacasova ◽  
...  
Keyword(s):  
T Cells ◽  
Adenylate Cyclase ◽  
Cd8 T Cells ◽  
In Vitro Activation

scholarly journals In vitro activation of theSaccharomyces cerevisiaeRas/adenylate cyclase system by glucose and some of its analogues

FEBS Letters ◽  
1991 ◽  
Vol 290 (1-2) ◽  
pp. 43-48 ◽  
Author(s):  
Luis Angel Pardo ◽  
Luis Maria Sánchez ◽  
Pedro S. Lazo ◽  
Sofia Ramos
Keyword(s):  
Adenylate Cyclase ◽  
Adenylate Cyclase System ◽  
In Vitro Activation

Cytochemical Evidence for Presynatic β-Adrenergic Regulation of Secretion in the Developing Rat Submandibular Gland

1977 ◽  
Vol 35 ◽  
pp. 430-431
Author(s):  
L.S. Cutler
Keyword(s):  
Cyclic Amp ◽  
Adenylate Cyclase ◽  
Submandibular Gland ◽  
Neonatal Rat ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Parotid Glands ◽  
Adrenergic Agonist ◽  
Rat Submandibular Gland

Many studies previously have shown that the B-adrenergic agonist isoproterenol and the a-adrenergic agonist norepinephrine will stimulate secretion by the adult rat submandibular (SMG) and parotid glands. Recent data from several laboratories indicates that adrenergic agonists bind to specific receptors on the secretory cell surface and stimulate membrane associated adenylate cyclase activity which generates cyclic AMP. The production of cyclic AMP apparently initiates a cascade of events which culminates in exocytosis. During recent studies in our laboratory it was observed that the adenylate cyclase activity in plasma membrane fractions derived from the prenatal and early neonatal rat submandibular gland was retractile to stimulation by isoproterenol but was stimulated by norepinephrine. In addition, in vitro secretion studies indicated that these prenatal and neonatal glands would not secrete peroxidase in response to isoproterenol but would secrete in response to norepinephrine. In contrast to these in vitro observations, it has been shown that the injection of isoproterenol into the living newborn rat results in secretion of peroxidase by the SMG (1).

Epinephrine Induces von Willebrand Factor Release from Cultured Endothelial Cells: Involvement of Cyclic AMP-dependent Signalling in Exocytosis

1997 ◽  
Vol 77 (06) ◽  
pp. 1182-1188 ◽  
Author(s):  
Ulrich M Vischer ◽  
Claes B Wollheinn
Keyword(s):  
Endothelial Cells ◽  
Adenylate Cyclase ◽  
Von Willebrand Factor ◽  
Umbilical Vein ◽  
Free Calcium ◽  
Camp Content ◽  
Von Willebrand ◽  
Willebrand Factor

Summaryvon Willebrand factor (vWf) is released from endothelial cell storage granules after stimulation with thrombin, histamine and several other agents that induce an increase in cytosolic free calcium ([Ca2+]i). In vivo, epinephrine and the vasopressin analog DDAVP increase vWf plasma levels, although they are thought not to induce vWf release from endothelial cells in vitro. Since these agents act via a cAMP-dependent pathway in responsive cells, we examined the role of cAMP in vWf secretion from cultured human umbilical vein endothelial cells. vWf release increased by 50% in response to forskolin, which activates adenylate cyclase. The response to forskolin was much stronger when cAMP degradation was blocked with IBMX, an inhibitor of phosphodiesterases (+200%), whereas IBMX alone had no effect. vWf release could also be induced by the cAMP analogs dibutyryl-cAMP (+40%) and 8-bromo-cAMP (+25%); although their effect was weak, they clearly potentiated the response to thrombin. Epinephrine (together with IBMX) caused a small, dose-dependent increase in vWf release, maximal at 10-6 M (+50%), and also potentiated the response to thrombin. This effect is mediated by adenylate cyclase-coupled β-adrenergic receptors, since it is inhibited by propranolol and mimicked by isoproterenol. In contrast to thrombin, neither forskolin nor epinephrine caused an increase in [Ca2+]j as measured by fura-2 fluorescence. In addition, the effects of forskolin and thrombin were additive, suggesting that they act through distinct signaling pathways. We found a close correlation between cellular cAMP content and vWf release after stimulation with epinephrine and forskolin. These results demonstrate that cAMP-dependent signaling events are involved in the control of exocytosis from endothelial cells (an effect not mediated by an increase in [Ca2+]i) and provide an explanation for epinephrine-induced vWf release.

Maternal and Fetal Platelet Responses and Adrenoceptor Binding Characteristics

1985 ◽  
Vol 53 (01) ◽  
pp. 095-098 ◽  
Author(s):  
C R Jones ◽  
R McCabe ◽  
C A Hamilton ◽  
J L Reid
Keyword(s):  
Adenylate Cyclase ◽  
Venous Blood ◽  
Adenosine Diphosphate ◽  
Binding Characteristics ◽  
Receptor Coupling ◽  
Threshold Response ◽  
Alpha Receptors ◽  
Maternal Responses ◽  
Epidural Anaesthetic

SummaryPaired blood samples were obtained from mothers (venous) and babies (cord venous blood) at the time of delivery by caesarean section under epidural anaesthetic. Fetal platelets failed to aggregate in response to adrenaline in vitro although adrenaline could potentiate the threshold response to adenosine diphosphate (1 μM). Fetal platelet responses to collagen and 8 Arg vasopressin did not differ significantly from maternal responses. Maternal and fetal platelets also showed similar inhibition of aggregation after activation of adenylate cyclase (PGE1 and parathormone), in contrast to the inhibition of adenylate cyclase by adrenaline.Alpha2 adrenoceptors were investigated using [3H] yohimbine binding receptor number and were reduced modestly but significantly on fetal compared to maternal platelets. The failure of fetal platelet aggregation in response to adrenaline appears to be related to a failure of receptor coupling and may represent a delayed maturation of fetal platelet alpha receptors or a response- to increased circulating catecholamines during birth.

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