Stimulated Flow of Pancreatic and Biliary Secretions after Intestinal Exposure to Cholera Toxin

1976 ◽  
Vol 51 (1) ◽  
pp. 81-85
Author(s):  
I. Freiman ◽  
R. N. Melmed

1. Duodenojejunal intestinal loops in rats were perfused with cholera toxin and the pancreatic and biliary secretory responses studied. 2. Intraluminal cholera toxin induced a significant flow of pancreatic and biliary ñuid and sustained protein (enzyme) secretion in pancreatic juice, in addition to the expected stimulation of mucosal secretion. 3. Intravenously injected cholera toxin failed to elicit a secretory flow from the pancreas and biliary tract. 4. The time-course of the enhanced secretory flow from pancreas and biliary tract after intraluminal cholera toxin corresponds closely to the secretion of intestinal fluid. 5. The results of these studies provide evidence of sustained stimulation of pancreatic and biliary secretions after mucosal exposure to cholera toxin. These observations support the suggestion that secretion from the pancreas and liver may significantly contribute to the total intestinal secretion in cholera.

1986 ◽  
Vol 116 (8) ◽  
pp. 1540-1546 ◽  
Author(s):  
Shin-Ichi Fukuoka ◽  
Masahiro Tsujikawa ◽  
Tohru Fushiki ◽  
Kazuo Iwai

1957 ◽  
Vol 190 (3) ◽  
pp. 403-407 ◽  
Author(s):  
Sherman R. Dickman ◽  
Gene A. Morrill

Mouse pancreas has been incubated in vitro with the parasympathomimetic drugs pilocarpine and Carbachol and with the hormones pancreozymin and secretin. The first three substances stimulated both respiratory rate and rate of enzyme secretion whereas secretin stimulated only the respiratory rate. The time-course of stimulation by pancreozymin was followed. Its effect on the respiratory rate was immediate while the largest secretion of ribonuclease occurred after 30 minutes of incubation. The secretory and respiratory effects of pancreozymin were not decreased by atropine but were slightly lessened by banthine. Large differences were found in the nonstimulated extrusion of ribonuclease in different strains of mice.


1992 ◽  
Vol 68 (05) ◽  
pp. 545-549 ◽  
Author(s):  
W L Chandler ◽  
S C Loo ◽  
D Mornin

SummaryThe purpose of this study was to determine whether different regions of the rabbit vascular system show variations in the rate of plasminogen activator (PA) secretion. To start, we evaluated the time course, dose response and adrenergic specificity of PA release. Infusion of 1 µg/kg of epinephrine stimulated a 116 ± 60% (SD) increase in PA activity that peaked 30 to 60 s after epinephrine administration. Infusion of 1 µg/kg of norepinephrine, isoproterenol and phenylephrine had no effect on PA activity. Pretreatment with phentolamine, an alpha adrenergic antagonist, blocked the release of PA by epinephrine while pretreatment with the beta blocker propranolol had no effect. This suggests that PA release in the rabbit was mediated by some form of alpha receptor.Significant arterio-venous differences in basal PA activity were found across the pulmonary and splanchnic vascular beds but not the lower extremity/pelvic bed. After stimulation with epinephrine, PA activity increased 46% across the splanchnic bed while no change was seen across the lower extremity/pelvic bed. We conclude that several vascular beds contribute to circulating PA activity in the rabbit, and that these beds secrete PA at different rates under both basal and stimulated conditions.


1993 ◽  
Vol 69 (3) ◽  
pp. 953-964 ◽  
Author(s):  
P. W. Glimcher ◽  
D. L. Sparks

1. The first experiment of this study determined the effects of low-frequency stimulation of the monkey superior colliculus on spontaneous saccades in the dark. Stimulation trains, subthreshold for eliciting short-latency fixed-vector saccades, were highly effective at biasing the metrics (direction and amplitude) of spontaneous movements. During low-frequency stimulation, the distribution of saccade metrics was biased toward the direction and amplitude of movements induced by suprathreshold stimulation of the same collicular location. 2. Low-frequency stimulation biased the distribution of saccade metrics but did not initiate movements. The distribution of intervals between stimulation onset and the onset of the next saccade did not differ significantly from the distribution of intervals between an arbitrary point in time and the onset of the next saccade under unstimulated conditions. 3. Results of our second experiment indicate that low-frequency stimulation also influenced the metrics of visually guided saccades. The magnitude of the stimulation-induced bias increased as stimulation current or frequency was increased. 4. The time course of these effects was analyzed by terminating stimulation immediately before, during, or after visually guided saccades. Stimulation trains terminated at the onset of a movement were as effective as stimulation trains that continued throughout the movement. No effects were observed if stimulation ended 40–60 ms before the movement began. 5. These results show that low-frequency collicular stimulation can influence the direction and amplitude of spontaneous or visually guided saccades without initiating a movement. These data are compatible with the hypothesis that the collicular activity responsible for specifying the horizontal and vertical amplitude of a saccade differs from the type of collicular activity that initiates a saccade.


1988 ◽  
Vol 167 (6) ◽  
pp. 1963-1968 ◽  
Author(s):  
L S Gray ◽  
J Gnarra ◽  
E L Hewlett ◽  
V H Engelhard

Cholera toxin (CT), but not pertussis toxin (PT), treatment of cloned murine CTL inhibited target cell lysis in a dose-dependent fashion. The effects of CT were mimicked by forskolin and cyclic adenosine monophosphate (cAMP) analogues. Inhibition of cytotoxicity by CT and cAMP analogs was mediated in part by attenuation of conjugate formation. Additionally, both CT and cAMP analogs blocked the increase in intracellular Ca2+ induced by stimulation of the TCR complex by mAbs. These findings indicate that cAMP inhibits the activity of CTL by two distinct mechanisms and suggests a role for this second messenger in CTL-mediated cytolysis.


1981 ◽  
Vol 16 (3) ◽  
pp. 377-384 ◽  
Author(s):  
J. Cassuto ◽  
M. Jodal ◽  
R. Tuttle ◽  
O. Lundgren

1996 ◽  
Vol 318 (2) ◽  
pp. 723-728 ◽  
Author(s):  
Michel PUCEAT ◽  
Guy VASSORT

Phospholipase Cγ (PLCγ) expression and activation by a purinergic agonist were investigated in adult rat cardiomyocytes. PLCγ is expressed in isolated cardiomyocytes. Stimulation of cells with extracellular ATP induces a rapid increase in membrane-associated PLCγ immunoreactivity most probably due to redistribution of the lipase from the cytosol to the membrane. The purine triggers a significant phosphorylation on tyrosine residues of a cytosolic pool of PLCγ with a time course that correlates with that of translocation. Extracellular ATP also increases intracellular Ins(1,4,5)P3 content. All these events (translocation and phosphorylation of PLCγ, InsP3 formation) are blocked by genistein, a tyrosine kinase inhibitor. The purinergic effect on both PLCγ translocation and phosphorylation are Ca-sensitive. We thus propose that the purinergic stimulation activates a non-receptor tyrosine kinase that phosphorylates PLCγ in the presence of an increased Ca level and induces PLCγ redistribution to the membrane. There, PLCγ becomes activated leading to the hydrolysis of phosphatidylinositol diphosphate and in turn Ins(1,4,5)P3 formation. This cascade of events may play a significant role in the induction of arrhythmogenesis by purinergic agonists.


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