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Biomedical subjects

K F Sewing

Publications and source records attributed to K F Sewing.

At least 199 records · Page 11Linked to original sources
PubMed1977

Effect of cimetidine on gastric mucosal histamine and histidine decarboxylase activity in rats.

In conscious rats and in anaesthetized gastric fistula rats, the effects of low and high doses of the histamine H2-receptor antagonist cimetidine was studied on gastric mucosal histamine concentration and histidine decarboxylase activity with or without concomitant administration of pentagastrin. In conscious animals a singleinjection of pentagastrin reduced gastric mucosal histamine concentration and elevated histidine decarboxylase activity. This effect was not antagonized by low doses of cimetidine. High doses of cimetidine, like pentagastrin, reduced the histamine concentration and elevated the histidine decarboxylase activity. In anaesthetized rats low doses of cimetidine and reduced gastric acid secretion. The effects of cimetidine on gastric mucosal histamine and histidine decarboxylase were less pronounced than in conscious animals. The histidine decarboxylase stimulating activity of high doses of cimetidine was not abolished by gastric perfusion with acid suggesting that endogenously released gastrin is not involved. A feedback relationship between the blockade of the target organ and increased histamine biosynthesis is discussed.

Acute Disease↗
PubMed1977

Methylation of histamine in the gastric mucosa.

Methylation of histamine in the gastric mucosa of various species has been studied in vitro and in vivo. When gastric mucosal homogenates of rat, guinea pig, cat, dog, and pig were incubated with 14C-histamine in the presence of S-adenosyl methionine Ntau-methylhistamine was formed as the only methylated histamine derivative. Excessive concentration of Ntau-methylhistamine inhibited the formation of Ntau-methylhistamine. Pretreatment of guinea pigs with prednisolone, aminoguanidine, or pentagastrin neither influenced in vitro the formation of Ntau-methylhistamine significantly nor shifted the methylation reaction towards the side chain. Pretreatment of guinea pigs with the histamine H2-receptor blocker cimetidine significantly enhanced the formation of Ntau-methylhistamine in vitro. In pooled samples of guinea pig gastric mucosa histamine and Ntau-methylhistamine were found. Under none of these circumstances was Nalpha-methyl-or Nalpha,Nalpha-dimethylhistamine found. It is concluded that in rat (to a small extent), guinea pig, cat, dog, and pig gastric mucosa the formation of Ntau-methylhistamine is the only methylating pathway of histamine. In cases where other methylated histamine derivates (Nalpha-methyl- and/or Nalpha,Nalpha-dimethylhistamine) are found they must origin in sources other than the gastric mucosa.

Animals↗
PubMed1976

Adenylate cyclase of the dog gastric mucosa: stimulation by histamine and inhibition by metiamide.

The activity of the non-stimulated, basal adenylate cyclase of the dog gastric mucosa is reduced by the histamine H2-receptor antagonist metiamide but not by the histamine H1-receptor antagonist mepyramine. Histamine activates the adenylate cyclase only slightly. In the presence of 10(-5) M metiamide a concentration-dependent stimulation of the enzyme by histamine was found. These data indicate that endogenous histamine in dog gastric mucosal homogenate is contributing at least in part to what is measured as "basal" adenylate cyclase activity. This effect is mediated by H2-receptor excitation and in earlier studies has prevented the demonstration of a stimulatory effect of exogenous histamine on this enzyme.

Adenylyl Cyclases↗
PubMed1975

Adenylate cyclase and phosphodiesterase in the rat gastric mucosa after starvation, feeding and pentagastrin.

The effects of starvation, feeding and pentagastrin on gastric mucosal adenylate cyclase (AC) and phosphodiesterase (PDE) activity were studied in the rat. 1. Starvation for 24 hrs and 48 hrs reduced both NaF stimulated and basal AC activities. 2. Feeding of starved rats slowly raised the AC activity up to 430% within 4 hrs after feeding. This effect was more pronounced under basal conditions than with NaF stimulation. 3. A single i.p. injection of pentagastrin (125 mug/kg) caused a stimulation of basal AC lasting 45 min, which was followed by a subsequent decrease in the basal and NaF stimulated enzyme activity. 4. PDE activity was not influenced by starvation and feeding but underwent a transient inhibition by pentagastrin. Accordingly gastric mucosal cAMP levels after starvation, feeding and pentagastrin are regulated by changes in AC and not in PDE activity. The rise in AC activity after feeding appears to be related to functions other than H+ and pepsin secretion.

Adenylyl Cyclases↗
PubMed1975

Effect of histamine H2-receptor and beta-receptor blockade on histamine-, orciprenaline- and prostaglandin-stimulated frequency of the isolated guinea-pig atrium.

For the oxyntic cell of the stomach the hypothesis was forwarded by Grossmann and Konturek [1] that, if one of its three receptors is blocked, the physico-chemical properties of the two others are changed in such a way that they respond less sensitively to their specific stimulation. This hypothesis was tested for the heart by studying the effect of histamine-H2-receptor- and beta-receptor-blockade on the orciprenaline-, histamine-, and prostaglandin E1-stimulated frequency of the spontaneously beating isolated guinea-pig atrium. Therefore cumulative dose response curves were established for orciprenaline, histamine and prostaglandin E1 (PGE1) alone or in the presence of metiamide or pindolol. (1) The beta-blocker pindolol inhibited the effect of orciprenaline in a competitive manner, without having an effect on histamine- and PGE1-stimulation. (2) The histamine H2-receptor blocker metiamide inhibited the histamine response competitively. (3) In contrast to pindolol, metiamide inhibited the PGE1-stimulated rise in atrial frequency, most obviously non- or uncompetitively. From these results it is evident that in the heart the particular inhibitors, at least at the receptor site, act rather specifically without affecting neighbouring receptors and that metiamide influences the PGE1-response in a way different from the receptor site.

Animals↗
PubMed1975

The effect of brocresine (NSD-1055) on basal and stimulated gastric acid secretion in chickens.

The effect of the histidine decarboxylase inhibitor 4-bromo-3-hydroxybenzyloxyamine-dihydrogenphosphate (brocresine, NSD-1055) on basal and histamine-, pentagastrin- and carbachol-stimulated gastric acid secretion was investigated in unanaesthetized gastric fistula chickens. Basal secretion was initially reduced by brocresine for 45 min and then slightly stimulated for 90 min. The histamine stimulated gastric secretion was competitively inhibited by brocresine. The acid response to low doses of pentagastrin and carbachol was enhanced, that to high doses unchanged. The results can be explained in the light of the assumption that a metabolic product of brocresine, 3-hydroxy-4-bromo-benzyl-alcohol stimulates gastric acid secretion.

Animals↗