Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The participation of carbonic anhydrase (CA II) in the gastric acid secretory process has been the subject of considerable controversy. We utilized a cDNA probe for CA II to measure CA II gene expression in canine gastric parietal cells that had been stimulated with the three principal acid secretagogues, carbachol, gastrin, and histamine. Hybridization to dot blots of total parietal cell RNA showed a significant increase in specific CA II mRNA content within minutes of secretagogue addition: carbachol stimulation led to an increase of 52 +/- 8.9%, reaching a maximum within 20 min; gastrin stimulation led to an increase within 60 min of 104 +/- 10.6%; stimulation with histamine was followed within 20 min by an increase of 30 +/- 7.2%. We also measured transcription rates for the CA II gene in cells stimulated by each agent and found an increase within 15 min. Our results show that CA II gene expression is regulated by agents that stimulate the parietal cell to secrete acid and that the accumulation of CA II mRNA subsequent to the initial interaction of stimulant appears to result from new transcription of the CA II gene. These data suggest the participation of CA II in the acid secretory response of the parietal cell to secretagogues.
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PMID:Carbonic anhydrase II gene expression in isolated canine gastric parietal cells. 246 11

The activity of gastric parietal cells in terms of hydrochloric acid (HCl) secretion is regulated by the interaction of stimulatory substances (e.g. gastrin) and inhibitors (e.g. somatostatin) acting in an endocrine and paracrine mode, as well as luminal factors. In the present study the following parameters were measured: the synthesis (mRNA), storage (tissue peptide concentration) and secretion (plasma peptide concentration) of somatostatin and gastrin following short-term treatment of rats with pentagastrin (acid stimulant), secretin, omeprazole (reduces gastric acidity by inactivating gastric H/K ATPase) and the somatostatin analogue octreotide (reduces gastric acidity by inhibiting both the parietal cell and gastrin). The mRNA coding for H/K ATPase and carbonic anhydrase II (CA II), the two enzymes responsible for the generation of hydrogen ions from the parietal cell, were also quantitated. In response to octreotide, somatostatin peptide and mRNA levels in the fundus rose to 180 +/- 16% (P < 0.001) and 1073 +/- 356% (P < 0.05) of control, respectively. In contrast, octreotide caused a decrease in antral somatostatin peptide and its mRNA did not change significantly. No significant changes in synthesis, secretion or storage of gastrin were observed except for omeprazole induced hypergastrinaemia (580 +/- 76%, P < 0.001). H/K ATPase and CA II mRNA were largely unaffected except for an increase in CA II mRNA following octreotide and a decrease in H/K ATPase mRNA after pentagastrin. These data support the concept of the differential control of antral and fundic somatostatin synthesis and provide evidence for a regulatory loop by which somatostatin can influence its own synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Secretory and biosynthetic responses of gastrin and somatostatin to acute changes in gastric acidity. 852 6