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Biomedical subjects

F Tárnok

Publications and source records attributed to F Tárnok.

6 recordsLinked to original sources
PubMed1979

The energy systems of gastric tissues, their neural, hormonal and pharmacological regulations in order to gastric H+ secretion and ulcerogenesis. (A review of animal experiments and clinical biochemical studies).

In studies conducted over the last 10 years, the ATP, ADP, AMP concentrations, the adenylate pool (ATP + ADP + AMP), the "energy charge" and the cAMP levels were determined:(1) in gastric tissues of pylorus-ligated rats, (2) in gastric and duodenal mucosa and muscular layer (musculature) of human subjects qualified as "hypacid", "normacid" and "hyperacid" on the basis of basal (BAO) and maximal acid output (MAO), (3) in ulcer-bearing and non-ulcerous antral, duodenal and jejunal mucosa and muscular layer of patients with peptic ulcer, including chronic (essential) antral, duodenal ulcer and jejunal ulcer following gastric resection of Billroth II-type. Close analysis of the results centres on: (1) the biochemical background of gastric hypersecretion and of ulcerogenesis in pylorus-ligated rats;(2) the extra- and intracellular feedback system operating between the gastric membrane ATPase and adenylate cyclase systems, under normal and abnormal conditions of the effector organ; (3) questions related to the regulatory mechanisms of functional activity of the effector organ under drug effect; (4) the energy structure of the mucosa and muscular layer of corpus ventriculi, antrum and duodenum in patients considered "hypacid", "normacid" and "hyperacid" on the grounds of the BAO and MAO values; (5) the interrelationships between human gastric H+--K+-dependent ATPase system of gastric corpus mucosa; (6) pharmacological regulation of the ATP--ADcer-free mucosa and musculature of patients with antral, duodenal and jejunal ulcers.

Adenosine Diphosphate↗
PubMed1979

The role of the ATP--adenylate cyclase--cAMP system and its pharmacological regulation in the development of gastric hypersecretion and ulceration.

The role and pharmacological regulation of the ATP-adenylate-cyclase--cAMP system were studied in the mucosa of the gastric fundus, and in the forestomach, of pylorus-ligated rats to elucidate the development of gastric hypersecretion and ulceration. (1) cAMP content of the tissue of the fundus mucosa and of the forestomach decreased before the significant increase of gastric H+ output and ulcer development; (2) the gastric H+ outputs depended on the breakdown of ATP in the fundus mucosa; (3) the gastric H+ secretion was inhibited in a dose-dependent way by theophylline, epinephrine and cimetidine; (4) the inhibition of gastric H+ secretion by epinephrine , theophylline or epinephrine plus theophylline associated with a significant increase in the mucosal cAMP of the gastric fundus (5) the significant increase in gastric H+ secretion due to histamine associated with a significant decrease in fundic mucosal cAMP; (6) the gastric H+ secretion could be inhibited dose-dependently by ADP, AMP, cyclic 2', 3'-AMP and cAMP; (7) the inhibition of gastric H+ secretion by cimetidine developed without and with histamine application in pylorus-ligated rats; (8) the histamine on gastric H+ secretion could not be stimulated further with theophylline (9) no significant correlation was found between the mucosal cAMP level and the gastric H+ secretion and/or between the decrease of mucosal cAMP content and gastric H+ secretion. It has been concluded that in pylorus-ligated rats (1) the gastric H+ secretion is an ATP-dependent process; (2) the cAMP system has an inhibitory effect as regards the development of gastric hypersecretion and of ulceration; (3) histamine and cimetidine show no close correlation with the cAMP system; (4) an extracellular and intracellular feed-back mechanism system exists between th ATP-membrane-bound ATPase-ADP and the ATP--adenylate cyclase--cAMP systems in the background of the development of gastric hypersecretion and ulceration.

Adenosine Diphosphate↗
PubMed1979

A comparative molecular--pharmacological study of drugs inhibiting Na+--K+-dependent ATPase separated from human gastric fundic mucosa. (One receptor system and more drugs).

The inhibitory effects of atropine, epinephrine, cyclic 3', 5'-AMP (cAMP), the prostaglandins E1 (PGE1) and E2 (PGE2) pentagastrin, histamine and ouabain have been studied on the activity of Na+--K+-dependent ATPase obtained from human gastric fundic mucosa. This study compares the sensitivity of the enzyme to a variety of drugs, applying the law of one receptor and more drugs. It was found that (1) the doses of drugs necessary to produce 50% inhibition to Na+--K+-dependent ATPase activity (affinity, pD2 value) significantly differ from each other C (atropine, 9.50; epinephrine, 8.60; cAMP: 11.30; PGE1, 9.30; PGE2, 9.45; pentagastrin, 9.45; histamine, 9.70 and ouabain, 9.50); (2) the intrinsic activities of drugs to Na+--K+-dependent, ATPase in comparison with ouabain (alpha=1.00) differ: atropine, PGE1, PGE2 and histamine, 1.00; pentagastrin, 0.87; cAMP, 0.48 and epinephrine, 0.41; (3) the inhibitory effects of different drugs, on Na+--K+-dependent ATPase system, depend on the magnitude of enzyme activity from human gastric fundic mucosa. It has been concluded that (1) the sensitivity of these drugs to the Na+--K+-dependent ATPase system and to the adenylate cyclase system, both obtained from human gastric mucosa, significantly differs from each other; (2) the main effect of pentagastrin and histamine on human gastric secretory function differs from the function of Na+--K+-dependent ATPase system; (3) the role of Na+--K+-dependent ATPase system and of adenylate cyclase can be separated pharmacologically from the point of view of human gastric H+ secretion.

Atropine↗
PubMed1979

Biochemical and energetic gradients in the mucosa of stomach and duodenum of patients with antral ulcer.

Separation and measurement of adenine-adenosine, adenosine monophosphate (AMP), adenosine diphosphate (ADP), adenosine triphosphate (ATP), lipid phosphates, RNA and DNA, further, separation and measurement of Mg2+-dependent, total (Mg2+-dependent plus Na+--K+-dependent, Mg2+-Na+-K-dependent) and Na+-K+-dependent ATPases were carried out in the mucosa and muscles of the corpus, antrum and duodenum of 68 patients with antral ulcer. It was found that (1) the substrate levels of adenosine nucleotides, lipid phosphates and RNA were significantly higher in the corpus mucosa than those in the mucosa of the antrum and duodenum (calculated for 1.0 mg DNA content); (2) the amounts of adenosine nucleotides and the sum of ATP + ADP + AMP did not alter significantly in the muscles of the corpus, antrum and duodenum; (3) the levels of adenosine nucleotides, sum of ATP + ADP + AMP, lipid phosphates and RNA, further the activities of Mg2+-dependent , total (Mg2/-dependent plus Na+-K+-dependent) and Na+-K+-dependent ATPases were significantly higher in the corpus mucosa than those in the corpus muscles. It was concluded that (1) energetic and biochemical gradients are present between the substrate levels in the mucosa of the corpus, antrum and duodenum; (2) the neural and/or humoral regulatory mechanisms differ in the mucosa and muscles of the corpus, in order to their biochemistry.

Adenine Nucleotides↗
PubMed1978

Interrelationships between the gastric secretory responses, prostaglandin E2 inhibition and serum level of immunoreactive gastrin in pylorus-ligated and antrectomized rats.

The effects of prostaglandin E2 (PGE2) have been studied on the gastric secretion and the serum level of immunoreactive gastrin in pylorus-ligated and antrectomized rats. It has been observed that: (1) a significant inhibition of gastric secretion (volume and acid output) was caused by PGE2, applied in doses of 75, 150 and 300 microgram/kg body weight, subcutaneously, in both pylorus-occluded and antrectomized rats: PGE2 inhibition of gastric secretion was more pronounced in rats with antrectomy; (2) no significant changes were found in the serum gastrin levels of both pylorus-ligated and antrectomized rats, and (3) no significant changes in serum levels of immunoreactive gastrin were produced by different doses of PGE2, in comparison with their marked inhibitory effects on gastric H+ secretion. It was concluded that there is no essential role of the immunoreactive gastrin, originated from the antral part of the stomach, neither in development of gastric hypersecretion nor in PGE2-produced inhibition on gastric secretion of the pylorus-occluded rats.

Animals↗