Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Calcitonin (CT) inhibits gastric acid and pancreatic enzyme secretion when infused intravenously. Therefore, in two patients showing excessively elevated CT-blood levels due to medullary thyroid carcinoma and in two patients with bone diseases before and under CT-treatment, gastric and pancreatic secretion were measured. Spontaneous (BAO) and pentagastrin stimulated acid as well as hormonally stimulated pancreatic enzyme secretion revealed normal in all subjects and tests. The findings are in favour of adaptation mechanisms of gastric parietal and pancreatic acinar cells against the inhibitory action of chronically elevated CT. Therefore, long term treatment with CT is no likely to induce impaired acidity or exocrine pancreatic insufficiency.
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PMID:[Gastric and exocrine pancreatic function in patients with medullary thyroid carcinoma and with bone diseases under treatment with calcitonin (author's transl)]. 70 15

The effects of acetazolamide, calcitonin (CT), and parathyroid hormone (PTH) on acid production in isolated osteoclasts has been investigated. Osteoclasts were isolated from the endosteum of 3-week chick tibias and were maintained under culture conditions for 5 days. The cells were treated with acetazolamide (10 x 4 M and 10(-7) M), CT (1 mU/ml and 0.31 mU/ml) and PTH (6.5 U/ml and 0.40 U/ml) for 1, 3, 6, and 18 hr. The cells were stained with acridine orange and the intensity of fluorescence measured by a light microscope photometer. Acetazolamide treatment resulted in a steady decline in intracellular acidity, suggesting that carbonic anhydrase plays a major role in acid production in isolated osteoclasts. Treatment with PTH produced a decline in acidity at 1 hr, followed by a peak at 3 hr and then a decline at 6 and 18 hr. The transient increase in acidity may be due to activation of carbonic anhydrase by PTH. Calcitonin treatment also resulted in a decline in cell acidity which was similar, but less pronounced than that resulting from acetazolamide treatment. These results indicate that calcitonin may mediate osteoclast activity by alterations in intracellular acid production.
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PMID:Characterization of isolated and cultured chick osteoclasts: the effects of acetazolamide, calcitonin, and parathyroid hormone on acid production. 314 73