Biomedical subjects
Publications and source records attributed to H J Ruoff.
Adenylate cyclase activity of human fundic mucosa is log-normally distributed and equally stimulated by pentagastrin and histamine. Cimetidine inhibits the histamine, but not the pentagastrin effect, which is even intensified by H2-receptor blockade. The results indicate that pentagastrin and histamine activate adenylate cyclase via distinct receptors.
Explore the source record for details and available documents.
The effect of adrenergic stimulation and blockade on the concentration of cAMP and cGMP was studied in the rat gastric mucosa. Adrenaline (0.5-2.0 mg/kg) elevated the gastric mucosal cAMP and cGMP levels up to 100% in a dose-dependent manner. Blockade of the beta-adrenoceptors with 4 mg/kg propranolol suppressed the adrenaline effect on the cAMP level and increased the effect on the cGMP concentration up to 500%. The opposite effect was found under alpha-adrenoceptor blockade. Phenoxybenzamine, 4 mg/kg, prevented the adrenaline effect on the cGMP level and increased the effect on the cAMP concentration up to 300%. Predominant stimulation of the beta-adrenoceptors by isoproterenol or of the alpha-adrenoceptors by phenylephrine caused smaller changes in the cyclic nucleotide concentration than did adrenaline. Their effect was more pronounced when the non-stimulated receptor was blocked. The data indicate that the rat gastric mucosa contains alpha- and beta-adrenoceptors. The effect of adrenaline on the gastric mucosal cAMP level is mediated by beta-adrenoceptors and that on the cGMP level by alpha-adrenoceptors.
Explore the source record for details and available documents.
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.
The presence and production of cyclic 3', 5'-adenosine monophosphate (cAMP) were investigated in the hypothalamus and neural lobe of the rat. Theophylline (concentrations from 10(-3) to 8 X 10(-3) M) increased the in vitro content of cAMP in the isolated neural lobe and in hypothalamic tissue samples containing supraoptic (SO) or paraventricular (PV) nuclei. Acetylcholine (ACH; 10(-2) and 10(-4) M) or carbachol (10(-4) M) did not increase cAMP content in the isolated neural lobe. Small increases were apparent (p less than 0.05, t-test for paired samples) in the hypothalamus. The amounts of cAMP were significantly higher in isolated neural lobes but not in hypothalami of NaCl-treated or lactating as compared to control rats. Presence of cAMP in the neural lobe and activation of adenylate cyclase under stimulated hormone release conditions indicate a possible involvement of cAMP in the process of neurohypophysial hormone secretion.
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.
The rates of disappearance of urotensin I, a peptide with a prolonged vasodepressor action, was studied in perfused isolated organs of the rat and in rat blood in vitro. The rates ranged from 29.9+/-3.2% in the perfused hind limb to 55.1 +/- 7.2% in the lungs. Urotensin I activity disappeared slowly during incubation with rat blood, the "half-life" being about 4 min. The fast removal or urotensin I by the organs contrasts with its long duration of action.
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.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.