Regulation of rat stomach histidine decarboxylase activity by the serum gastrin concentration

1973 ◽  
Vol 3 (3) ◽  
pp. 178-179 ◽  
Author(s):  
R. Håkanson ◽  
G. Liedberg ◽  
J. Oscarson ◽  
J. F. Rehfeld ◽  
F. Stadil
Keyword(s):  
Histidine Decarboxylase ◽  
Serum Gastrin ◽  
Decarboxylase Activity ◽  
Rat Stomach ◽  
Serum Gastrin Concentration ◽  
Histidine Decarboxylase Activity

scholarly journals Correlation between serum gastrin concentration and rat stomach histidine decarboxylase activity

1974 ◽  
Vol 243 (2) ◽  
pp. 483-498 ◽  
Author(s):  
R. Håkanson ◽  
J. H. Kroesen ◽  
G. Liedberg ◽  
J. Oscarson ◽  
J. F. Rehfeld ◽  
...  
Keyword(s):  
Histidine Decarboxylase ◽  
Serum Gastrin ◽  
Decarboxylase Activity ◽  
Rat Stomach ◽  
Serum Gastrin Concentration ◽  
Histidine Decarboxylase Activity

Development of sensitivity to different secretagogues in the rat stomach

1983 ◽  
Vol 244 (2) ◽  
pp. G165-G170
Author(s):  
M. Ikezaki ◽  
L. R. Johnson
Keyword(s):  
Acid Secretion ◽  
Histidine Decarboxylase ◽  
Decarboxylase Activity ◽  
Pepsin Secretion ◽  
Rat Stomach ◽  
Naturally Occurring ◽  
Comprehensive Picture ◽  
Basal Acid ◽  
Old Rats ◽  
Histidine Decarboxylase Activity

Acid and pepsin secretion and gastric mucosal histidine decarboxylase activity were measured in rats of various ages between 5 and 40 days after injection of saline, pentagastrin, histamine, or carbachol. Basal acid secretion first appeared on day 15. At this time carbachol significantly stimulated both acid and pepsin secretion. Gastrin and histamine did not stimulate acid or pepsin secretion until day 20. Histidine decarboxylase activity first appeared on day 10 and was first increased by pentagastrin on day 18. Injection of 8-day-old rats with corticosterone prematurely induced acid secretion on day 12 in response to all three stimulants and pepsin secretion in response to carbachol only. These studies provide a comprehensive picture of the development of gastric mucosal sensitivity to the three naturally occurring stimulants and indicate that adrenal glucocorticoids play an important role in that development.

Rat stomach ECL-cell histidine decarboxylase activity is suppressed by ergocalciferol but unaffected by parathyroid hormone and calcitonin

1999 ◽  
Vol 79 (2-3) ◽  
pp. 131-139 ◽  
Author(s):  
Rebecca Gagnemo-Persson ◽  
Per Persson ◽  
Tomas Bryngelsson ◽  
Britt Greén ◽  
Rolf Håkanson
Keyword(s):  
Parathyroid Hormone ◽  
Histidine Decarboxylase ◽  
Decarboxylase Activity ◽  
Rat Stomach ◽  
Ecl Cell ◽  
Histidine Decarboxylase Activity

Ischemia of rat stomach mobilizes ECL cell histamine

2005 ◽  
Vol 288 (5) ◽  
pp. G1084-G1090 ◽  
Author(s):  
Masayuki Kitano ◽  
Maria Bernsand ◽  
Yosuke Kishimoto ◽  
Per Norlén ◽  
Rolf Håkanson ◽  
...  
Keyword(s):  
Histidine Decarboxylase ◽  
Ischemia Reperfusion ◽  
Celiac Artery ◽  
Enzyme Linked Immunosorbent Assay ◽  
Decarboxylase Activity ◽  
Rat Stomach ◽  
Ecl Cells ◽  
Ecl Cell ◽  
Mucosal Lesions ◽  
Histidine Decarboxylase Activity

Microdialysis was used to study how ischemia-evoked gastric mucosal injury affects rat stomach histamine, which resides in enterochromaffin-like (ECL) cells and mast cells. A microdialysis probe was inserted into the gastric submucosa, and the celiac artery was clamped (30 min), followed by removal of the clamp. Microdialysate histamine was determined by enzyme-linked immunosorbent assay. In addition, we studied the long-term effects of ischemia on the oxyntic mucosal histidine decarboxylase activity in omeprazole-treated rats. Gastric mucosal lesions induced by the ischemia were enlarged on removal of the clamp. The microdialysate histamine concentration increased immediately on clamping (50-fold rise within 30 min) and declined promptly after the clamp was removed. In contrast, histidine decarboxylase activity of the ECL cells was lowered by the ischemia and returned to preischemic values 9 days later. Mast cell-deficient rats responded to ischemia-reperfusion much like wild-type rats with respect to histamine mobilization. Pretreatment with the irreversible inhibitor of histidine decarboxylase, α-fluoromethylhistidine, which is known to eliminate histamine from ECL cells, prevented the rise in microdialysate histamine. Pharmacological blockade of acid secretion (cimetidine or omeprazole) prevented the lesions induced by ischemia-reperfusion insult but not the mobilization of histamine. In conclusion, ischemia of the celiac artery mobilizes large amounts of histamine from ECL cells, which occurs independently of the gross mucosal lesions. The prompt reduction of the mucosal histidine decarboxylase activity in response to ischemia probably reflects ECL cell damage. The lesions develop not because of mobilization of histamine per se but because of ischemia plus reperfusion plus gastric acid.

scholarly journals Effect of hydrocortisone on histidine decarboxylase activity in rat stomach.

1988 ◽  
Vol 36 (10) ◽  
pp. 4088-4094 ◽  
Author(s):  
NORIAKI IMANISHI ◽  
EIJI OHMORI ◽  
KIMIO YATSUNAMI ◽  
ATSUSHI ICHIKAWA
Keyword(s):  
Histidine Decarboxylase ◽  
Decarboxylase Activity ◽  
Rat Stomach ◽  
Histidine Decarboxylase Activity
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