Adrenergic stimulation of isolated rat gastric mucosal cells

1982 ◽  
Vol 320 (2) ◽  
pp. 175-181 ◽  
Author(s):  
H.-J. Ruoff ◽  
M. Wagner ◽  
Christine Günther ◽  
S. Maśliński
1975 ◽  
Vol 78 (2) ◽  
pp. 392-400
Author(s):  
Arne T. Hostmark ◽  
Ole Grønnerød ◽  
Robert S. Horn

ABSTRACT The antagonism between insulin and selective adrenergic stimulation on the converting systems for glycogen synthetase and phosphorylase has been investigated in the isolated rat diaphragm. Insulin significantly inhibited stimulation by terbutaline and noradrenaline of phosphorylase b to a conversion as well as stimulation of glycogen synthetase I to D conversion by these agents. The inhibition by insulin was stronger on the synthetase system than on the phosphorylase system. The insulin effect was not dependent upon the presence of glucose. In diaphragms from 24 h fasted rats the response of the phosphorylase system to both agonists decreased. Inhibition by insulin of terbutaline stimulated phosphorylase conversion was maintained upon fasting while no effect of insulin against stimulation by noradrenaline could be obtained in diaphragms from fasted rats. The effects of fasting and insulin were not influenced by beta adrenergic antagonists (practolol and butoxamine). The results indicate a difference in sensitivity of the synthetase and phosphorylase systems to insulin and suggest that noradrenaline and terbutaline influence glycogen metabolism by differing mechanisms.


1985 ◽  
Vol 249 (2) ◽  
pp. G197-G202 ◽  
Author(s):  
G. M. Short ◽  
G. M. Reel ◽  
J. W. Doyle ◽  
M. M. Wolfe

The present studies were directed toward examining the effects of gastrin-releasing peptide (GRP) on acid secretion and on beta-adrenergic-stimulated gastrin and somatostatin release using the isolated vascularly perfused rat stomach. Including pentagastrin in perfusion buffer increased acid output from 2.2 +/- 0.4 mueq H+/h during control perfusion to 18.8 +/- 1.8 mueq H+/h (P less than 0.01). No significant changes in acid secretion were detected when either GRP or specific antibodies to GRP were included in perfusate in the absence or presence of pentagastrin. Inclusion of 10(-9) M isoproterenol in the perfusate did not change acid output with respect to control; however, gastrin and somatostatin release into the portal venous effluent was significantly enhanced. Peak gastrin and somatostatin concentrations observed at 15 min were 753 +/- 43% (P less than 0.001) and 345 +/- 43% (P less than 0.01), respectively, of basal levels. When antibodies to GRP were included in perfusate containing isoproterenol, gastrin and somatostatin release into the portal venous effluent was significantly inhibited. The results of these studies indicate that GRP does not affect basal or pentagastrin-stimulated gastric acid secretion in the isolated perfused rat stomach. However, under the conditions of these experiments, beta-adrenergic stimulation of gastrin and somatostatin release appears to be mediated, at least in part, through GRP.


1985 ◽  
Vol 16 (3-4) ◽  
pp. 202-204 ◽  
Author(s):  
H. -J. Ruoff ◽  
K. Reutter ◽  
W. Schepp

FEBS Letters ◽  
1980 ◽  
Vol 120 (1) ◽  
pp. 80-84 ◽  
Author(s):  
Mary C. Sugden ◽  
Ann F.C. Tordoff ◽  
Vera Ilic ◽  
Dermont H. Williamson

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