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Biomedical subjects

H Kather

Publications and source records attributed to H Kather.

At least 109 records · Page 6Linked to original sources
PubMed1980

Effects of salbutamol and butoxamine on the human fat cell adenylate cyclase.

In order to characterize the beta-adrenoceptors coupled to the human fat cell adenylate cyclase more extensively the effects of the beta 2-selective agonist salbutamol on basal and isoproterenol-stimulated rates of cAMP-accumulation were studied. Although exhibiting only low intrinsic activity salbutamol displayed only slightly lower affinity towards the beta-adrenoceptors linked to the human fat cell adenylate cyclase than isoproterenol. In addition, the beta 2-selective antagonist butoxamine was slightly more potent in inhibiting the isoproterenol-stimulated fat cell enzyme than the cardioselective beta-blocking agent practolol. These results further emphasize the difficulties in classifying the lipolytic response of adipose tissue to beta-adrenergic agonists and antagonists within a uniform beta-receptor theory.

Adenylyl Cyclases↗
PubMed1980

Interaction of laxatives with enzymes of cyclic AMP metabolism from human colonic mucosa.

The mechanism by which laxatives such as dioctyl sodium sulfosuccinate and ricinoleic acid evoke colonic fluid secretion has been suggested to involve mucosal cyclic AMP. Ricinoleic acid and dioctyl sodium sulfosuccinate were tested for their capacity to modulate the key enzymes of cAMP-metabolism--adenylate cyclase and cAMP-phosphodiesterase--in human colonic mucosa. Both laxatives were ineffective stimuli of human colonic adenylate cyclase. In contrast to ricinoleic acid, dioctyl sodium sulfosuccinate was a competitive inhibitor of soluble cAMP-phosphodiesterase activity. These experiments suggest that the cathartic properties of dioctyl sodium sulfosuccinate in human colonic mucosa might be mediated by cyclic AMP via inhibition of soluble phosphodiesterase activity.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1980

Inhibition of human fat cell adenylate cyclase mediated via alpha-adrenoceptors.

Human adipose tissue contains alpha- as well as beta-adrenoceptor sites mediating antagonistic catecholamine effects on lipolysis. To characterize the mechanisms of catecholamine action in biochemical terms we have studied the effects of the almost pure beta-adrenoceptor agonist isoproterenol and of the mixed adrenergic agonist adrenaline on human fat cell adenylate cyclase in the presence of alpha- and beta-adrenoceptor blocking drugs. In contrast to the almost pure beta-adrenergic agent isoproterenol, the mixed agonist adrenaline, besides its stimulatory action, also had inhibitory effects which became apparent upon complete beta-adrenoceptor blockade using 0.05 mmol/l propranolol. Under these conditions adrenaline caused a dose-dependent inhibition of basal and parathyroid hormone-activated enzymic activity with a maximum of 30-50%, which was dependent on GTP and could be reversed by simultaneous alpha-adrenergic blockade using 5 mumol/l dihydroergotamine or 10 mumol/l phentolamine. These results support the concept of antogonistic alpha- and beta-adrenoceptor sites coexisting as regulatory subunits of the human fat cell adenylate cyclase.

Adenylyl Cyclase Inhibitors↗
PubMed1980

Human gastric mucosal adenylate cyclase activity: effects of various cytoprotective prostaglandins.

Several prostaglandins prevent ulcer formation (called cytoprotection) by a mechanism other than inhibition of gastric acid secretion. One suggestion is that they increase cyclic AMP in non-parietal cells. A variety of prostaglandins with potent cytoprotective properties were tested for their capacity to modulate adenylate cyclase activity in homogenates of human gastric mucosa. Prostaglandin E2, prostacyclin (PGI2) and 15(S)-methyl-PGE2 stimulated the cyclase in human gastric mucosal biopsy specimens in a dose-dependent manner. Cytoprotective prostaglandins without antisecretory properties such as PGF2 beta were also able to activate the enzyme system dose-dependently. In contrast, cytoprotective prostaglandins such as PGD2, the PGE1-analogue, SC-29333, and the prostaglandin-like compound C83 did not stimulate human gastric adenylate cyclase. Whereas PGD2 did not modulate enzyme activity at all, SC-29333 and C83, at concentrations greater than 10 mumol/l, inhibited basal and PGE2-stimulated enzyme activities. These studies suggest that cyclic AMP is not directly related to the cytoprotective effect of prostaglandins, at least in human gastric mucosa.

Adenylyl Cyclases↗
PubMed1980

Human colonic adenylate cyclase. Stimulation of enzyme activity by vasoactive intestinal peptide and various prostaglandins via distinct receptor sites.

The effects of meclofenamic acid on basal and hormone-stimulated adenylate cyclase in human colonic mucosa were tested. It is shown that meclofenamic acid is a relatively specific inhibitor of the stimulatory action of prostaglandins on the level of mucosal adenylate cyclase. This compound did not inhibit significantly the effects of vasoactive intestinal peptide (VIP) on the human enzyme system. VIP18-28 did not act as a partial agonist and did not inhibit the response to the intact VIP. Our studies suggest the existence of distinct receptor sites for both secretagogues (VIP and prostaglandins) in human colonic mucosa.

Adenylyl Cyclases↗
PubMed1980

PGI2-sensitive human adenylate cyclase in biopsy specimens of corpus, antral and duodenal mucosa.

The distribution of prostacyclin-(PGI2-)sensitive cyclase in human gastric and duodenal mucosa was studied. Like PGE2, PGI2 induced a dose-dependent increase of enzyme activity throughout the stomach and the duodenum. Maximal effects (about 2.5- to 3.0-fold increase) were observed at a PGI2 concentration of 0.28 mmol/l. The stable breakdown product 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) was much less active. The equal distribution of the PGI2-sensitive adenylate cyclase in the human upper alimentary tract suggests a localization of this enzyme system in cells not directly related to gastric acid secretion.

Adenylyl Cyclases↗
PubMed1980

[Influence of ranitidine on antipyrine metabolism (author's transl)].

Antipyrine kinetics were determined in 6 healthy volunteers before and after the end of a 1 week treatment period of ranitidine 150 mg twice a day. The mean antipyrine half-life (h) was before 12.6 +/- 4.6 h and after ranitidine treatment 12.0 +/- 2.6 h. Antipyrine clearance (ml/min) and volume of distribution (1) were not altered following ranitidine administration. The results suggest that ranitidine has no influence on antipyrine-metabolism in healthy volunteers.

Adult↗
PubMed1980

[Clinical aspects of cytoprotection with prostaglandin analogs].

Various prostaglandins posses antisecretory and cytoprotective actions on gastric mucosa. Cytoprotection by prostaglandins is unrelated to the inhibition of gastric acid secretion and can also be detected in small intestinal mucosa of the rat. Prostaglandins protect gastric mucosa against ulcerogenic compounds such as nonsteriod anti-inflammatory agents (NOSAC) as well as against the necrotizing affect produced by alcohol, 25% sodium chloride, 0.2 N solium hydroxide and 0.6 N hydrochloride acid. Prostaglandins protect in doses that are far too small to inhibit gastric acid secretion. At these doses no side-effects have been noted so far. This cytoprotective effect of prostaglandins might be beneficial in the treatment of a variety of diseases in which gastric mucosal injury in present.

Animals↗
PubMed1979

[Inhibition of pentagastrin-stimulated gastric secretion by ranitidine (author's transl)].

The dose-effect relationship of ranitidine, a recently developed selective histamine H2 receptor antagonist was tested on six healthy subjects after oral administration. Ranitidine gave dose-dependent inhibition of pentagastrin-stimulated acid secretion. Half-maximal inhibition occurred at 75 mg. The antisecretory effect was still demonstrable five hours after oral intake. The drug is thus more powerful and has more lasting antisecretory action, even after oral intake, than cimetidine.

Adult↗
PubMed1979

[Peptic ulcer disease and primary hyperparathyroidism (author's transl)].

The causal relationship of primary hyperparathyroidism and ulcer disease is reviewed. In contrast to earlier ideas careful clinical and clinico-chemical investigations have shown that in patients with manifest primary hyperparathyroidism neither is the incidence of ulcer disease raised nor are deviations from the normal behavior of acid secretion or the serum gastrin level to be observed in comparison with the average population.

Calcium↗