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Biomedical subjects

H J Ruoff

Publications and source records attributed to H J Ruoff.

At least 37 records · Page 2Linked to original sources
PubMed1985

Prostaglandin formation by isolated gastric parietal and nonparietal cells of the rat.

Rat gastric cells isolated by pronase and subdivided by Percoll into 3 fractions (F1, F2, F3) were used to study prostaglandin E2 (PGE2) formation and, as an indirect measure of parietal cell H+ production, [14C]-aminopyrine uptake. Cells that had not been fractionated, with 20 to 25% parietal cells, contained at 0 degree C 1.7 +/- 0.35 (s.e.mean) ng PGE2 10(8) cells-1. During incubation at 37 degrees C these cells steadily synthesized up to 4.36 +/- 0.73 ng PGE2 10(8) cells-1 from endogenous substrate. Indomethacin in concentrations higher than 10(-6) mol 1(-1) inhibited this basal formation completely, but 10(-4) mol 1(-1) did not reduce the cellular PGE2 level below 1.4 +/- 0.2 ng 10(8) cells-1. Arachidonic acid in concentrations higher than 10(-5) mol 1(-1) evoked an abundant formation of PGE2, and 10(-4) mol 1(-1) built up a plateau of over 7.5 +/- 1.65 ng PGE2 10(8) cells-1 within 15 min. PGE2 formation in cell fractions increased significantly with the number of parietal cells per assay tube. Indomethacin (10(-8) to 10(-4) mol 1(-1] did not influence the histamine-stimulated uptake of [14C]-aminopyrine, while arachidonic acid (10(-5) to 10(-4) mol 1(-1] inhibited this process. PGE2 formation in response to arachidonic acid was prevented by indomethacin, but the inhibition of aminopyrine uptake by arachidonic acid could not be prevented by indomethacin. The data suggest that isolated gastric cells of the rat sustain constant PGE2 synthesis in vitro, which is more pronounced in parietal than in mucosal and chief cells. PGE2 may exert different effects within distinct gastric cell types.

Aminopyrine↗
PubMed1984

Intrinsic factor secretion from isolated human gastric mucosal cells.

Human gastric mucosal cells were isolated from the resected fundic mucosa of peptic ulcer patients. The intracellular content and secretion of intrinsic factor were estimated by binding to cyano[57Co]cobalamin. The content was maximal in the enriched parietal cell fraction which also displayed the highest H+ production as measured by amino[14C] pyrine uptake. Secretagogues evoked full response after 15 min of incubation: pentagastrin (181% of basal secretion), carbachol (208%), histamine (250%) and dibutyryl cyclic adenosine monophosphate (304%). The phosphodiesterase inhibitor isobutylmethylxanthine was slightly more effective even than dibutyryl cAMP. The response to histamine was abolished by ranitidine, indicating activation of adenylate cyclase via histamine H2 receptors, but remained unaffected by atropine, which in turn blocked the carbachol effect, whereas ranitidine was ineffective. The mean formation rate was 8.4 fmol intrinsic factor/10(6) cells per h under basal conditions and 14.3 fmol in response to histamine.

1-Methyl-3-isobutylxanthine↗
PubMed1984

Potentiating action of hexoprenaline on 14C-aminopyrine uptake by isolated rat parietal cells.

Hexoprenaline potentiated the 14C-aminopyrine uptake (a reliable index of H+ generation) of isolated rat gastric cells stimulated by 10(-6) -10(-4) mol/l carbachol, and inhibited that in response to 10(-4) mol/l histamine without and in the presence of propranolol. It is concluded that hexoprenaline acts as a partial agonist on parietal cell H2-receptors and that beta-adrenoceptor activation may functionally modulate gastric acid secretion.

Aminopyrine↗
PubMed1984

Adenylate cyclase and H+ production of isolated rat parietal cells in response to glucagon and histamine.

The effect of glucagon and its interaction with histamine on adenylate cyclase (AC), cellular cAMP and [14C]aminopyrine ( [14C]AP) uptake, a reliable index of parietal cell H+ production, was studied in isolated rat gastric cells. AC activation in response to glucagon and histamine correlated with the number of parietal cells. Glucagon (10(-10)-10(-6) mol/l) increasingly stimulated AC (maximal effect: 92% by 10(-7) mol/l) and cellular cAMP (86% by 10(-9) mol/l) of fractions enriched with 80% parietal cells but did not cause a pronounced change of the histamine-stimulated enzyme. If there was any interaction, the effect of both hormones was additive. Glucagon neither changed basal [14C]AP uptake nor interfered with that in response to histamine. The data suggest that if glucagon activates a parietal cell AC this process is not followed by parietal cell H+ production. Furthermore, unlike other inhibitors such as somatostatin or PGE2, glucagon does not reduce acid secretion via the cAMP system of the parietal cell.

Adenylyl Cyclases↗
PubMed1984

Intrinsic factor secretion from isolated gastric mucosal cells of rat and man--two different patterns of secretagogue control.

Intrinsic Factor (IF) secretion was studied using isolated gastric mucosal cells from rat and man. In the rat, IF was localized to the chief cells and its secretion responded most efficaciously to carbachol. DbcAMP and hexoprenaline were less powerful, whereas histamine and pentagastrin lacked any effect. In man, IF secretion derived from the parietal cells and was increasingly enhanced by hexoprenaline, pentagastrin, carbachol, histamine and dbcAMP. In both species, IF secretion differs with respect to its cellular origin and the pattern of secretagogue control: IF release from rat chief cells is due to muscarinic receptor excitation, whereas IF release from human parietal cells responds predominantly to histamine-H2-receptor activation and seems to be mediated by the cAMP system.

Adenylyl Cyclases↗
PubMed1983

Cellular origin and release of intrinsic factor from isolated rat gastric mucosal cells.

The cellular content and secretion of intrinsic factor was measured by [57Co]cyanocobalamin binding using isolated rat gastric mucosal cells. The intrinsic factor/R-protein ratio was above 9:1 as evaluated by specific anti-intrinsic factor antibodies. In unfractionized cells with 23 +/- 1.3% parietal cells the intrinsic factor content of 148 +/- 47 fmol/10(6) cells remained almost unchanged over 3 h, whereas basal secretion rose up to 57 +/- 10. In fractionized cells (Percoll) with 3-85% parietal cells most intrinsic factor was found in the parietal cell-depleted fraction (content: 441 +/- 30, secretion/3 h: 139 +/- 16, mean formation/h: 50 +/- 12 fmol/10(6) cells). The intrinsic factor content of the different cell fractions correlated with that of pepsin. [14C]Aminopyrine uptake, an indirect measure of parietal cell H+ production, was inversely related. Carbachol (1 X 10(-6)-10(-3) mol/l) stimulated intrinsic factor secretion, 1 X 10(-3) mol/l being maximally effective (90 +/- 8% above basal). This response was inhibited by atropine and pirenzepine, but not by prostaglandin E2 (PGE2) and somatostatin. Dibutyryl cyclic adenosine monophosphate (dibutyryl cAMP, 43 +/- 7%) and hexoprenaline (24 +/- 5%) enhanced intrinsic factor secretion less effectively and pentagastrin like histamine lacked any stimulatory effect. We conclude that in the rat intrinsic factor is produced and released from chief cells mainly under cholinergic control.

Aminopyrine↗
PubMed1983

Comparison of the effect of PGE2 and somatostatin on histamine stimulated 14C-aminopyrine uptake and cyclic AMP formation in isolated rat gastric mucosal cells.

In isolated rat gastric cells somatostatin and PGE2 were compared in respect to their effects on the cAMP system and on the histamine-stimulated H+-production, measured by 14C-aminopyrine (14C-AP) uptake. Like PGE2 somatostatin activated adenylate cyclase (AC) for all in non-parietal cells. This effect on AC declined in cell fractions with increasing number of parietal cells. Activation of AC or elevation of cellular cAMP and uptake of 14C-AP in response to histamine were inhibited by 10(-9) to 10(-5) mol/1 PGE2 and somatostatin. The results indicate remarkable similarity between somatostatin and PGE2: both activate a non-parietal cell AC and both inhibit H+-production, likely by interfering at the histamine sensitive AC of the parietal cell.

Adenylyl Cyclases↗
PubMed1983

Adenylate cyclase in gastric mucosal biopsies from patients with achlorhydria. Stimulation by PGE2, histamine and gastrointestinal hormones.

Activation of adenylate cyclase (AC) by PGE2, histamine and gastrointestinal hormones was studied in parietal cell-free gastric biopsy specimens from the corpus of patients with proven high gastrin achlorhydria. PGE2, somatostatin, VIP, pentagastrin and secretin activated AC in a concentration-dependent manner both in normal and in atrophic mucosa. Histamine activated AC only in normal gastric mucosa, being entirely ineffective in mucosa devoid of parietal cells. The results indicate that histamine-sensitive AC disappears in patients with achlorhydria, probably due to their loss of parietal cells. Enzyme activity in response to somatostatin, VIP, pentagastrin, secretin and PGE2 remains unchanged in these patients indicating AC localization in nonparietal cells, e.g. chief or mucous cells.

Achlorhydria↗
PubMed1983

Aminopyrine accumulation of isolated parietal cells from the rat stomach. Effect of histamine and interaction with endogenous inhibitors.

The inhibitory properties of secretin, vasoactive intestinal polypeptide (VIP), cholecystokinin (CCK), somatostatin and prostaglandin E2 (PGE2) on acid production in response to histamine were tested in vitro by measuring the 14C-aminopyrine (14C-AP) uptake into isolated rat parietal cells, a reliable index of H+ generation. All compounds significantly inhibited 14C-AP accumulation and 4 X 10(-8) mol/l secretin, 7 X 10(-8) mol/l PGE2 and 2 X 10(-7) mol/l CCK decreased the effect of 10(-4) mol/l histamine by 50% (IC50). VIP and somatostatin did not reduce AP-uptake to such extent and the approximate IC50 values could not be established. The type of inhibition by all peptides and PGE2 appeared not to be competitive in nature. Our data suggest that these compounds inhibit acid production by a mechanism localized directly at the parietal cell and that secretin and CCK are unlikely to exert a physiological role as inhibitors of gastric acid secretion.

Aminopyrine↗
PubMed1982

Adrenergic stimulation of isolated rat gastric mucosal cells. Effect on adenylate cyclase and 14C-aminopyrine uptake.

Adrenergic stimulation of the adenylate cyclase (AC)-cAMP-system and 14C-aminopyrine accumulation, an indirect measure of parietal cell H+-production, was studied in a different preparations of gastric mucosal cells. The beta 2-adrenoceptor agonist hexoprenaline activated AC of crude homogenates from the gastric corpus of mouse, rat, guinea-pig, hog, dog and man. In isolated rat gastric cells (20% parietal cells), treated by low power sonication, 10(-8) to 10(-3) mol/l adrenaline and hexoprenaline activated AC equally potently and efficaciously by maximally 170%. Isoprenaline proved to be less effective activating up to 80%. 5.10(-5) mol/l GMP-PNP augmented basal activity 8.5 times and reduced the maximal efficacy. Adrenaline and hexoprenaline activated AC by maximally 120%, isoprenaline by 40%. The potency of adrenaline was 4 times lower, that of hexoprenaline 2 and that of isoprenaline 4 times higher in the presence of GMP-PNP. Adrenergic stimulation was inhibited by the beta-adrenoceptor antagonist propranolol, the effect of alpha-adrenoceptor-blockade by phenoxybenzamine was less pronounced. In fractions with 7-80% of parietal cells, prepared by isopycnic centrifugation with Percoll, adrenaline and hexoprenaline activated AC or hexoprenaline enhanced the cellular levels of cAMP in parietal cell poor and rich fractions. The degree of activation in response to histamine correlated with the number of parietal cells. 14C-Aminopyrine uptake was increasingly stimulated through 10(-8) to 10(-5) mol/l hexoprenaline, maximally by doubling the basal accumulation. 10(-4) mol/l histamine was 8 times more effective. 3.10(-7) mol/l propranolol inhibited the effect of 10(-5) mol/l hexoprenaline by 80%. The data suggest the localization of beta-adrenoceptors (likely beta 2-adrenoceptors) on parietal and other nonidentified gastric cells. At the parietal cell, adrenaline and hexoprenaline initiate activation of AC and hexoprenaline leads to H+-production. The responses are small compared to the effect of histamine. Thus, beta-adrenoceptor agonists exert intrinsic activity in relation to H+-production. Their influence on stimulated secretion of isolated cells remains to be elucidated.

Adenylyl Cyclases↗
PubMed1982

Inhibition by prostaglandin E2, somatostatin and secretin of histamine-sensitive adenylate cyclase in human gastric mucosa.

The effects of prostaglandin E2 (PGE2), somatostatin and secretin on gastric mucosal adenylate cyclase (AC) and their interactions with the histamine-sensitive AC were studied using biopsy specimens of normal human gastric mucosa. PGE2 (10(-7) to 10(-3) mol/l), somatostatin (10(-9) to 10(-5) mol/l), secretin (10(-9) to 10(-6) mol/l) and histamine (10(-7) to 10(-3) mol/l), all stimulated mucosal AC in a concentration-dependent manner. Besides this effect, PGE2, somatostatin and secretin significantly inhibited the histamine-activated enzyme at concentrations as low as 10(-10) to 10(-7) (PGE2), 10(-9) to 10(-6) (somatostatin) and 10(-9) to 10(-5) mol/l (secretin). They were more potent than cimetidine which initiated inhibition at concentrations exceeding 10(-7) mol/l. The data show that PGE2, somatostatin and secretin have a dual action on AC: (1) they all activate human gastric AC on their own, and (2) they all inhibit the histamine-sensitive enzyme at the parietal cell level at nanomolar concentrations, thus underlining the concept that hormonal control is essential in the regulation of gastric acid secretion.

Adenylyl Cyclase Inhibitors↗
PubMed1981

Adrenaline sensitive adenylate cyclase in human gastric mucosa.

Basal and adrenaline-stimulated adenylate cyclase (AC) was studied in biopsy specimens of the gastric and duodenal mucosa from 112 individuals. AC activities were log normally distributed. AC of fundic and antral gastric mucosa responded to adrenaline in a concentration-dependent manner, that of the duodenal mucosa did not respond to adrenaline. The degree of activation in biopsies of normal gastric mucosa was similar to that of patients with chronic atrophic gastritis or patients antrectomized according to the Billroth method. AC in biopsies from cimetidine-treated peptic ulcer patients was less sensitive to adrenaline than AC in biopsies from untreated patients. The threshold concentration of cimetidine to inhibit adrenaline-stimulated AC in vitro was 10(-6) mol/l. The data provide evidence of an adrenaline-sensitive AC in cells other than parietal cells and show an inhibitory action of cimetidine on the catecholamine-sensitive AC in the human gastric mucosa.

Adenylyl Cyclases↗
PubMed1981

Adenylate cyclase activity in gastric mucosal biopsies and cAMP in gastric juice before and after cimetidine treatment in healthy subjects.

Previous studies have revealed augmented parietal call sensitivity to histamine stimulation after cessation of cimetidine treatment in healthy subjects. To elucidate one possible mechanism for this effect, we measured cAMP in gastric mucosa and gastric juice during histamine stimulation in vivo and histamine-stimulated adenylate cyclase activity in vitro in biopsy material obtained by gastroscopy. In eight healthy subjects the cAMP content of gastric corpus mucosal biopsies was measured before, during, and after infusion of 2.5 and 25.6 microgram . kg-1 . h-1 of histamine dihydrochloride. No increase in cAMP content was found. In 10 healthy subjects cAMP secretion into gastric juice was studied before and 36 to 84 h after cessation of 4 weeks' treatment with cimetidine, 1 g/day. No significant increase of cAMP output was found in response to infusion of 2.5 and 25.6 microgram . kg-1 . h-1 of histamine dihydrochloride either before or after the treatment period. Thus histamine does not stimulate cAMP secretion into gastric juice in man. In the same 10 subjects histamine-stimulated adenylate cyclase activity was studied in vitro in biopsy material obtained before and 60 h after cessation of cimetidine treatment. The dose-response curve of the adenylate cyclase activity was not shifted to the left. The results indicate that the augmented parietal cell sensitivity to histamine, seen after stopping cimetidine treatment in healthy subjects, is not due to increased sensitivity of the adenylate cyclase-cAMP system to histamine stimulation.

Adenylyl Cyclases↗
PubMed1980

Effect of pentagastrin on gastric mucosal nucleic acid synthesis of fed guinea pigs.

In normally fed guinea pigs the effect of a sustained release pentagastrin preparation was studied on gastric mucosal weight, protein, DNA and RNA concentration and thymidine and uridine incorporation into DNA and RNA, respectively. Treatment with pentagastrin for 3 days significantly increased antral fundic mucosal DNA and RNA concentration and thymidine and uridine incorporation. It is concluded that pentagastrin stimulates gastric mucosal nucleic acid synthesis beyond the driving force elicited by food.

Animals↗
PubMed1979

Adenylate cyclase in human gastric mucosa: its activation by histamine in morphologically different biopsy specimens.

In morphologically different biopsy specimens from fundic, antral and duodenal mucosa of 134 persons, basal and histamine stimulated adenylate cyclase activity was studied: Basal and stimulated adenylate cyclase activities were log-normally distributed. Only in the fundic but not in the antral and duodenal mucosa adenylate cyclase was sensitive to histamine. The mean basal activity in the fundic gastric mucosa was 148, in response to 10(-5) mol/l histamine 292 pmol cAMP/mg protein/20 min. In human fundic biopsy specimens histologically identified as normal gastric mucosa, the stimulatory effect of histamine on adenylate cyclase decreased with the individual's age. In bioptic material from patients suffering from histologically proven chronic gastritis the histamine effect decreased with the degree of atrophy. A similar loss of histamine sensitivity was found in gastric mucosal biopsies of antrectomized individuals operated at least 5 years before by the Billroth I or II method, whereas in the mucosa of patients with gastric or duodenal ulcer no loss occurred. In contrast, the most pronounced stimulatory action of histamine was found in this latter group. Since a histamine sensitive adenylate cyclase is localized only in the glandular area of the fundic mucosa and the histamine sensitivity depends on a morphological intact structure of the mucosa, it can be concluded, that the effects of histamine on adenylate cyclase and on hydrochloric acid acid secretion have to be considered as a mechanism linked together.

Adenylyl Cyclases↗