Cl- requirement of acid secretion in isolated gastric glands

1983 ◽  
Vol 245 (4) ◽  
pp. G573-G581 ◽  
Author(s):  
D. H. Malinowska ◽  
J. Cuppoletti ◽  
G. Sachs
Keyword(s):  
Steady State ◽  
Acid Secretion ◽  
Parietal Cell ◽  
Acid Formation ◽  
Dibutyryl Camp ◽  
Steady State Distribution ◽  
State Distribution ◽  
Gastric Glands ◽  
Lateral Membrane ◽  
Isolated Gastric Glands

The dependence of acid formation, as measured by aminopyrine (AP) accumulation, on medium and intracellular Cl- was investigated in resting (10(-4) M cimetidine) and stimulated (10(-3) M dibutyryl cAMP) gastric glands isolated from the rabbit stomach. Intracellular Cl- concentrations (Cli-) were measured by the steady-state distribution of 36Cl-. In Cl- -free conditions AP accumulation was absent. Medium Cl- induced AP accumulation (AP ratio = 125) in stimulated glands with a K0.5 of 10.4 +/- 1.1 mM, equivalent to 18.0 +/- 1.2 mM Cli-, and had a small effect on resting glands (AP ratio = 6). With normal Nai+ and Ki+ maintained, similar results were obtained in stimulated glands treated with 10(-5) M amphotericin (ampho) and 10(-4) M ouabain (ouab), where the basal-lateral membrane was confirmed to be short-circuited with respect to Cl- pathways, i.e., medium Cl- and Cli- were equal. The K0.5 for Cl-i was 17.5 +/- 2.5 mM. In resting glands treated with ampho and ouab, AP accumulation increased linearly (no saturation was observed) with increasing Cl- (AP ratio = 35). These results suggest that stimulation activates a Cl- component in the secretory membrane and not in the basal-lateral membrane of the parietal cell. The K+ requirement of AP accumulation at a physiological Cl-i of 60 mM was also investigated in ampho- and ouab-treated glands. On stimulation the K0.5 for Ki+ decreased from 19.5 to 12 mM, coupled with a large increase in AP accumulation, indicating that stimulation also activates a K+ component in the secretory membrane.(ABSTRACT TRUNCATED AT 250 WORDS)

Inhibitory action of somatostatin on isolated gastric glands and parietal cells

1983 ◽  
Vol 245 (2) ◽  
pp. G221-G229 ◽  
Author(s):  
C. S. Chew
Keyword(s):  
Parietal Cell ◽  
Inhibitory Action ◽  
Parietal Cells ◽  
Acid Formation ◽  
Gastric Glands ◽  
Isolated Gastric Glands ◽  
Cell Acid ◽  
Kinetics Of ◽  
Apparent Ic50

The action of somatostatin in vitro was characterized using glands and parietal cells isolated from rabbit gastric mucosa. In the presence of the reducing agent dithiothreitol, somatostatin was found to inhibit gastrin- and histamine-stimulated acid formation in glands as measured by [14C]aminopyrine (AP) accumulation and oxygen consumption, both measurements that appear to be reliable indexes of parietal cell acid formation. In glands the inhibition of the secretory response to gastrin was more potent (60-80%) than that to histamine (15-25%). The kinetics of somatostatin inhibition of responses to both agents were noncompetitive. The apparent IC50 for the partial somatostatin inhibition of histamine-stimulated AP accumulation was similar to that for gastrin (approx 3 X 10(-9) M) when maximum concentrations of histamine (10(-4) M) or gastrin (10(-7) M) were used. The inhibitory action of somatostatin appeared to be specific, inasmuch as this peptide had no significant effect on basal secretion or secretion stimulated by carbachol, dibutyryl cAMP, cholera toxin, or elevated extracellular K+. In purified parietal cell preparations, somatostatin inhibited histamine- but not gastrin-stimulated AP accumulation. Moreover, the inhibition of histamine-stimulated AP accumulation in parietal cells was more pronounced than in glands. These results suggest that somatostatin acts directly on parietal cells to inhibit histamine activation of H+ secretion. Somatostatin also acts indirectly to inhibit gastrin, perhaps by blocking the release of histamine from paracrine- or endocrinelike cells present in the glands.

Lack of interaction between acid and pepsinogen secretion in isolated gastric glands

1983 ◽  
Vol 245 (6) ◽  
pp. G775-G779
Author(s):  
S. J. Hersey ◽  
M. Miller ◽  
D. May ◽  
S. H. Norris
Keyword(s):  
Cyclic Nucleotides ◽  
Acid Formation ◽  
Dibutyryl Camp ◽  
Gastric Glands ◽  
Isolated Gastric Glands ◽  
Pepsinogen Secretion ◽  
Inhibited Acid ◽  
Weak Stimulation ◽  
Stimulation Of

Gastric glands isolated from rabbit stomach were employed to study the relation between acid and pepsinogen secretion. The effects of adenosine and guanosine nucleotides were examined for both secretory processes. cAMP, dibutyryl cAMP (DBcAMP), and 8-bromo-cAMP (8BrcAMP) were found to stimulate both acid and pepsinogen secretion with a potency sequence of 8BrcAMP greater than DBcAMP greater than cAMP. Adenosine, ATP, and AMP were ineffective, indicating that the responses to adenosine cyclic nucleotides do not involve an adenosine receptor. 8BrcGMP was found to produce a weak stimulation of both acid and pepsinogen secretions, while GMP, cGMP, and DBcGMP were ineffective. DBcGMP was found to inhibit competitively the stimulation of pepsinogen secretion by cholecystokinin (CCK)-like peptides. No inhibition was found with cGMP or 8BrcGMP. Stimulation of pepsinogen secretion by carbachol or isoproterenol was not inhibited by DBcGMP nor was the stimulation of acid formation by CCK-like peptides. Thiocyanate inhibited acid formation but did not affect pepsinogen secretion stimulated by 8BrcAMP or carbachol, indicating that stimulation of pepsinogen secretion does not require simultaneous acid formation. Costimulation of acid formation by histamine and pepsinogen secretion by isoproterenol showed no interaction between the two secretory processes. The results are interpreted to suggest that correlations between acid and pepsinogen secretion observed in vivo do not result from direct interactions between parietal and chief cells.

Helicobacter pylori vacuolating cytotoxin (VacA) inhibits tubulovesicle fusion-possible mechanism for the inhibition of acid secretion in isolated gastric glands

2001 ◽  
Vol 120 (5) ◽  
pp. A652-A652
Author(s):  
S KARVAR ◽  
J DUMAN ◽  
X YAO ◽  
R ZHOU ◽  
T COVER ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Acid Secretion ◽  
Gastric Glands ◽  
Vacuolating Cytotoxin ◽  
Isolated Gastric Glands

Kinetic analysis of mechanism of intestinal Na+-dependent sugar transport

1985 ◽  
Vol 248 (5) ◽  
pp. C498-C509 ◽  
Author(s):  
D. Restrepo ◽  
G. A. Kimmich
Keyword(s):  
Experimental Data ◽  
Steady State ◽  
Sugar Transport ◽  
Enzyme Kinetic ◽  
Steady State Distribution ◽  
State Distribution ◽  
Least Squares Fit ◽  
Coupling Stoichiometry ◽  
Rate Limiting ◽  
Kinetics Of

Zero-trans kinetics of Na+-sugar cotransport were investigated. Sugar influx was measured at various sodium and sugar concentrations in K+-loaded cells treated with rotenone and valinomycin. Sugar influx follows Michaelis-Menten kinetics as a function of sugar concentration but not as a function of Na+ concentration. Nine models with 1:1 or 2:1 sodium:sugar stoichiometry were considered. The flux equations for these models were solved assuming steady-state distribution of carrier forms and that translocation across the membrane is rate limiting. Classical enzyme kinetic methods and a least-squares fit of flux equations to the experimental data were used to assess the fit of the different models. Four models can be discarded on this basis. Of the remaining models, we discard two on the basis of the trans sodium dependence and the coupling stoichiometry [G. A. Kimmich and J. Randles, Am. J. Physiol. 247 (Cell Physiol. 16): C74-C82, 1984]. The remaining models are terter ordered mechanisms with sodium debinding first at the trans side. If transfer across the membrane is rate limiting, the binding order can be determined to be sodium:sugar:sodium.

PROCESSOR SHARING G-QUEUES WITH INERT CUSTOMERS AND CATASTROPHES: A MODEL FOR SERVER AGING AND REJUVENATION

2017 ◽  
Vol 31 (4) ◽  
pp. 420-435 ◽  
Author(s):  
J.-M. Fourneau ◽  
Y. Ait El Majhoub
Keyword(s):  
Steady State ◽  
Product Form ◽  
Processor Sharing ◽  
Service Capacity ◽  
Steady State Distribution ◽  
State Distribution ◽  
Signal Arrival ◽  
Open Networks ◽  
Networks Of Queues

We consider open networks of queues with Processor-Sharing discipline and signals. The signals deletes all the customers present in the queues and vanish instantaneously. The customers may be usual customers or inert customers. Inert customers do not receive service but the servers still try to share the service capacity between all the customers (inert or usual). Thus a part of the service capacity is wasted. We prove that such a model has a product-form steady-state distribution when the signal arrival rates are positive.

Inhibition of acid secretion in isolated gastric glands by substituted benzimidazoles

1982 ◽  
Vol 243 (6) ◽  
pp. G505-G510 ◽  
Author(s):  
E. Fellenius ◽  
B. Elander ◽  
B. Wallmark ◽  
H. F. Helander ◽  
T. Berglindh
Keyword(s):  
Oxygen Consumption ◽  
Gastric Gland ◽  
Acid Formation ◽  
Gastric Glands ◽  
New Class ◽  
Weak Bases ◽  
Morphological Studies ◽  
Isolated Gastric Glands ◽  
Dose Dependent ◽  
Distal Site

A new class of gastric acid inhibitors, substituted benzimidazoles (H 83/69 and H 149/94), have been tested in an isolated rabbit gastric gland preparation. Acid formation in the glands was stimulated by histamine, dibutyryl cAMP (DBcAMP), and high extracellular K+ concentrations, and the glandular secretory response was measured by changes in oxygen consumption and in accumulation of the weak base [14C]aminopyrine (AP). The substituted benzimidazoles inhibited AP accumulation induced by all stimulants in a dose-dependent noncompetitive manner. In contrast, cimetidine only inhibited histamine-induced AP accumulation. Basal AP accumulation, not affected by cimetidine, was also inhibited by the substituted benzimidazoles, as was the increase in glandular oxygen consumption produced by the addition of histamine and DBcAMP. Basal oxygen consumption was inhibited by about 15%. The substituted benzimidazoles, like AP, are weak bases and were also found to accumulate in the glands. Semiquantitative morphological studies of glands stimulated by histamine plus theophylline did not show any change in the enlarged secretory surface area after stimulation in the presence of inhibitory concentrations of H 149/94 (10(-4) M). The results suggest that substituted benzimidazoles have a mechanism of action different from that of H2-receptor antagonists and indicate a very distal site of action in the events leading to acid formation.

Ontogeny of pepsin secretory response to secretagogues in isolated rat gastric glands

1986 ◽  
Vol 250 (2) ◽  
pp. G200-G204 ◽  
Author(s):  
J. Yahav ◽  
P. C. Lee ◽  
E. Lebenthal
Keyword(s):  
Term Neonate ◽  
Ionophore A23187 ◽  
Newborn Rats ◽  
Dibutyryl Camp ◽  
Gastric Glands ◽  
Cholecystokinin Octapeptide ◽  
Rat Pups ◽  
Isolated Gastric Glands ◽  
Old Rats ◽  
Isolated Rat

By use of isolated gastric glands from rats at various ages, we demonstrated that full-term neonate and 1-day-old rats showed no response to cholecystokinin octapeptide (CCK-OP), carbachol, or Ca2+ ionophore. The same glands, however, were responsive to dibutyryl cAMP. A mature response was not found until the pups were 2 days old. Injection of hydrocortisone into newborn rats led to an increase in pepsinogen concentrations in gastric glands and also an increased responsiveness to CCK-OP, carbachol, and Ca2+ ionophore A23187 24 h after administration. Hydrocortisone thus caused precocious maturation of both pepsinogen accumulation and pepsinogen secretory responsiveness of gastric glands in rat pups.

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