“…These antagonists have been characterized as competitive inhibitors of histamine-induced acid secretion and, moreover, inhibit pentagastrin or gastrin induced secretion in all species so far S E studied Parsons, 1973;Wyllie, Hesselbo & Black, 1972;Wyllie, Ealding, Hesselbo & Black, 1973).…”
SUMMARY1. The consequence of H2-receptor blockade for the secretary responses of the gastric mucosa to hormonal or cholinergic stimulation was studied in conscious rats with Heidenhain pouches or Pavlov pouches with the antrum retained or resected.2. Metiamide almost completely abolished acid secretion induced by pentagastrin without altering significantly the amount of histamine excreted in the urine. Histamine mobilization on pentagastrin infusion determined in vitro, seemed to be larger during H2-receptor blockade than with pentagastrin alone.3. CCK-PZ mobilized mucosal histamine to a considerable extent; the secretary response to this hormone was completely abolished by H2-receptor blockade.4. Acid secretion in response to 2-deoxy-D-glucose was inhibited by H2-receptor blockade in the presence or absence of the antrum; however the inhibition was less complete than with hormone-induced secretion.5. The acid secretary response to 100 mg/kg of 2-deoxy-D-glucose appeared to be less susceptible to H2-receptor blockade than that of 50 mg/kg of 2-deoxy-D-glucose.6. Feeding induced a secretary response in the Pavlov pouch which initially was more effectively inhibited by H2-receptor blockade than the response to 2-deoxy-D-glucose. In the absence of antral gastrin secretion by either stimulus was equally inhibited.7. Methacholine-induced acid secretion was inhibited by infusion of the H2-receptor antagonist, an inhibition that was absent when pentagastrin was concomitantly infused.8. Although acid secretion induced by cholinergic stimuli was readily inhibited by the H2-receptor antagonist, slight or no inhibition was noted on pepsin secretion.9. The role of histamine as a physiological stimulus for the parietal cell is discussed in view of the fact that the secretary effect of natural stimuli, known or demonstrated to mobilize mucosal histamine, is restrained by H.-receptor blockade.
“…These antagonists have been characterized as competitive inhibitors of histamine-induced acid secretion and, moreover, inhibit pentagastrin or gastrin induced secretion in all species so far S E studied Parsons, 1973;Wyllie, Hesselbo & Black, 1972;Wyllie, Ealding, Hesselbo & Black, 1973).…”
SUMMARY1. The consequence of H2-receptor blockade for the secretary responses of the gastric mucosa to hormonal or cholinergic stimulation was studied in conscious rats with Heidenhain pouches or Pavlov pouches with the antrum retained or resected.2. Metiamide almost completely abolished acid secretion induced by pentagastrin without altering significantly the amount of histamine excreted in the urine. Histamine mobilization on pentagastrin infusion determined in vitro, seemed to be larger during H2-receptor blockade than with pentagastrin alone.3. CCK-PZ mobilized mucosal histamine to a considerable extent; the secretary response to this hormone was completely abolished by H2-receptor blockade.4. Acid secretion in response to 2-deoxy-D-glucose was inhibited by H2-receptor blockade in the presence or absence of the antrum; however the inhibition was less complete than with hormone-induced secretion.5. The acid secretary response to 100 mg/kg of 2-deoxy-D-glucose appeared to be less susceptible to H2-receptor blockade than that of 50 mg/kg of 2-deoxy-D-glucose.6. Feeding induced a secretary response in the Pavlov pouch which initially was more effectively inhibited by H2-receptor blockade than the response to 2-deoxy-D-glucose. In the absence of antral gastrin secretion by either stimulus was equally inhibited.7. Methacholine-induced acid secretion was inhibited by infusion of the H2-receptor antagonist, an inhibition that was absent when pentagastrin was concomitantly infused.8. Although acid secretion induced by cholinergic stimuli was readily inhibited by the H2-receptor antagonist, slight or no inhibition was noted on pepsin secretion.9. The role of histamine as a physiological stimulus for the parietal cell is discussed in view of the fact that the secretary effect of natural stimuli, known or demonstrated to mobilize mucosal histamine, is restrained by H.-receptor blockade.
“…Cardiovascular effects following burimamide have also been seen in dogs (Lorenz, Thermann, Hamelmann, Schmal, Maroske, Reimann, Kusche, Schingale, Dormann & Keck, 1973). In man, Wyllie, Hesselbo & Black (1972) …”
Burimamide (34‐1080 μM) caused a concentration‐dependent increase in the force and frequency of contraction of kitten isolated atria.
Metiamide (467 μM) had no stimulant action on kitten atria and did not modify the effects of burimamide.
The atrial stimulation produced by burimamide was reduced by (‐)‐propranolol (34‐68 nM) and by cocaine (3 μM).
The atrial stimulant effect of burimamide was prevented by pretreatment of kittens with reserpine (1 mg/kg, 24 h before the experiment).
It is concluded that burimamide causes atrial stimulation by releasing catecholamines.
“…1), antagonize the stimulation of gastric secretion in man both by histamine and pentagastrin (Wyllie and Hesselbo, 1973). These mine in gastric secretion and have suggested that H2 receptor antagonists might have therapeutic value in the treatment of peptic ulcer.…”
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