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Biomedical subjects

H Hannemann

Publications and source records attributed to H Hannemann.

9 recordsLinked to original sources
PubMed1990

Interaction of calcium channel antagonists with parietal cell acid production, adenylate cyclase, intracellular-free Ca2+ and H+/K+-ATPase.

The calcium channel antagonists verapamil, gallopamil and nifedipine were tested for their effects on acid secretion stimulated by histamine and dibutyryl-cyclic AMP in isolated and enriched guinea pig parietal cells, on adenylate cyclase activity mediated by histamine H2 receptors, on histamine-stimulated increase in cytosolic-free Ca2+ concentration [Ca2+], on gastric H+/K(+)-ATPase activity and on H+/K(+)-ATPase-mediated proton uptake in intact gastric membrane vesicles. Verapamil and gallopamil impaired all cellular and enzymatic test systems studied. Both drugs affected with highest potency the acid secretion in the parietal cell preparation (IC50: 1-2 mumol/l) and the H+/K(+)-ATPase-mediated H+ uptake in gastric membrane vesicles, whereas their inhibitory action was less pronounced on adenylate cyclase and on histamine-induced increase in cytosolic-free [Ca2+]. The type of interaction found in the gastric membrane vesicle preparation indicates that both drugs act as protonophores. Nifedipine was less effective as an inhibitor of acid secretion in the parietal cell preparation and in reducing proton concentration in isolated gastric membrane vesicles. The drug failed to block adenylate cyclase and H+/K+-ATPase activity. Since nifedipine is a more effective calcium channel blocking agent but a less lipophilic drug than verapamil and gallopamil, we conclude that the antisecretory activity of calcium channel antagonists in vitro is mediated by a nonspecific, i.e. a protonophoric, action. We suggest that verapamil exhibits its antisecretory activity in vivo partially by its protonophoric action at the secretory membrane of the parietal cell, whereas the decrease in acid secretion by nifedipine is not mediated by this mechanism.

Adenosine Triphosphatases↗
PubMed1989

Arachidonic acid metabolism in isolated gastric mucous and parietal cells.

Arachidonic acid metabolism was studied in isolated gastric mucous and parietal cells. During a 90 min incubation, mucous cells incorporated [1-14C]arachidonic acid (4.5 mumol/l) into triacylglycerols (500 pmol/mg protein), phosphatidylcholine (520), phosphatidylethanolamine (290) and phosphatidylinositol (100). 230 pmol/mg protein was recovered as 14CO2 and 130 pmol/mg protein in the form of unidentified water-soluble metabolites. The incorporation rates were linearly related with arachidonic acid concentration up to 10 mumol/l. Neither equimolar concentrations of oleic acid, palmitic acid and linoleic acid nor prostaglandin E2 (1 mumol/l) or indomethacin (10 mumol/l) affected incorporation. During prolonged incubation incorporated arachidonic acid was transferred from triacylglycerols and phosphatidylcholine to phosphatidylethanolamine. Upon subcellular fractionation most of the incorporated arachidonic acid was found in the microsomal fraction. Compared with mucous cells, parietal cells incorporated arachidonic acid less quickly into phospholipids, but utilized it more efficiently for energy metabolism. In conclusion gastric cells show a highly dynamic metabolism of arachidonic acid which is qualitatively similar but quantitatively different between cell types.

Animals↗
PubMed1988

Interaction of antidepressants and neuroleptics with histamine stimulated parietal cell adenylate cyclase and H+ secretion.

The tricyclic antidepressants trimipramine and doxepin, and the neuroleptic agents trifluoperazine and haloperidol were tested for their effect on histamine H2-receptor-mediated adenylate cyclase activity and H+ secretion in guinea-pig parietal cells. All compounds inhibited histamine-stimulated adenylate cyclase and H+ secretion in a concentration-dependent manner. The antisecretory potency was 1-2 orders of magnitude higher than that for adenylate cyclase inhibition. All drugs caused a rightward shift in the concentration-response curves of histamine-induced adenylate cyclase activation with Schild-plot lines having a slope significantly different from unity. Histamine-stimulated H+ secretion was inhibited by the drugs in a noncompetitive fashion. These results demonstrate that antidepressants and neuroleptics interfere noncompetitively with the parietal cell histamine H2-receptor and that this receptor blocking activity is not related to the antisecretory activity of the drugs.

Adenylyl Cyclases↗
PubMed1988

Comparative pharmacology of histamine H2-receptor antagonists.

There was no significant difference between the concentration-dependent inhibitory effects produced by roxatidine acetate, roxatidine and ranitidine on adenylate cyclase derived from isolated and enriched guinea-pig parietal cells. All the compounds shifted the concentration-response curve of histamine to the right and transformation of this data to Schild-plots produced straight lines with slopes greater than 1 but not significantly different from each other. The pA2 values characterising the potencies were roxatidine acetate 6.85 +/- 0.86, roxatidine 7.14 +/- 0.04, and ranitidine 6.92 +/- 0.01. Histamine-stimulated acid production from isolated guinea-pig parietal cells, measured by the 14C-aminopyrine accumulation technique, was similarly affected by the 3 compounds. Schild-plot slopes of roxatidine acetate and ranitidine were not significantly different from unity and pA2 values were similar to those of the adenylate cyclase inhibition, roxatidine acetate 7.15 +/- 0.09, roxatidine 7.03 +/- 0.02, and ranitidine 6.83 +/- 0.10. In conclusion, roxatidine acetate and its major metabolite roxatidine behave like competitive antagonists with potencies similar to ranitidine on H2-receptors on the guinea-pig parietal cell.

Histamine H2 Antagonists↗
PubMed1986

Interaction of ranitidine and famotidine with guinea pig-isolated parietal cells.

The inhibitory effects of the histamine H2-receptor antagonists, ranitidine and famotidine on histamine-stimulated gastric acid secretion have been studied in guinea pig isolated, enriched parietal cells using the 14C-aminopyrine accumulation technique. The 14C-aminopyrine accumulation curves in response to histamine were shifted towards the right in a parallel fashion by ranitidine, and in a nonparallel fashion by famotidine. The inhibitory effect of ranitidine, but not that of famotidine, was readily reversed by washing the parietal cells. It is concluded that the histamine H2-receptors in guinea pig parietal cells are blocked competitively and reversibly by ranitidine, but noncompetitively and partially reversibly by famotidine.

Animals↗
PubMed1985

The adenylate cyclase-cyclic AMP-protein kinase system in different cell populations of the guinea pig gastric mucosa.

In isolated guinea pig gastric mucous and enriched parietal cells it was tested whether or not cyclic AMP in response to histamine stimulation might reach concentrations sufficiently high to activate an intracellular cyclic AMP-dependent protein kinase and thereby mediate the acid response. Although histamine stimulated parietal cell adenylate cyclase to a greater extent than mucous cell adenylate cyclase, cyclic AMP levels in response to maximal histamine stimulation reached higher levels in mucous than in parietal cells. This had to be attributed to a five times higher phosphodiesterase activity in parietal cell than in mucous cell populations. In the absence of the phosphodiesterase inhibitor isobutylmethylxanthine exposure of the cells to histamine only in mucous cells produced an increase in cyclic AMP-dependent protein kinase activity ratio, but not in parietal cells. Dibutyryl-cyclic AMP induced cyclic AMP accumulation in parietal cell populations was compared to dibutyryl-cyclic AMP induced H+ secretion, as measured by 14C-aminopyrine uptake. A maximal acid response was associated with an intracellular cyclic AMP level of approximately 300 pmol/10(6) cells, which was never reached by maximal histamine stimulation even not in the presence of the phosphodiesterase inhibitor. It is concluded that activation of the parietal cell cyclic AMP-dependent protein kinase is one way for stimulating H+ secretion, but that the acid response elicited by histamine requires another intracellular pathway.

Adenylyl Cyclases↗
PubMed1977

[Optimum delivery methods in breech presentation].

In 581 cases of breech presentation during the years 1966--1974 in 90% of cases delivery was possible vaginally. We prefered the method of Lövset und Veit-Smellie. Casarian section was performed in 9,5% of the cases, the mortality of the newborns was 14%. Without the premature newborns (less than 1000 gr), the cases of intrauterine deaths and not viable children with malformations the mortality was 5,6%. The perinatal mortality of the children or more than 2500 gr was merely 0,69%. The general enlargement of the indication for Caesarian section is not recommended.

Adult↗
PubMed1976

[On the optimal method of delivery in breech presentation (author's transl)].

Between 1966 and 1974, 90% of 581 single breech presentations were delivered vaginally. The incidence of Caesarean Section was 9.5%. The overall perinatal mortality was 14%. After elimination of premature deliveries under 1000 grams, stillbirth prior to labour and non-viable anomalies, the perinatal mortality was 5.6%. The perinatal mortality in infants over 2500 grams was 0.69%.

Birth Weight↗