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.

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)

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.

Stimulation of pepsinogen secretion in permeable isolated gastric glands

1985 ◽  
Vol 249 (3) ◽  
pp. G408-G415
Author(s):  
S. H. Norris ◽  
S. J. Hersey
Keyword(s):  
Lactate Dehydrogenase ◽  
Gastric Glands ◽  
Cholecystokinin Octapeptide ◽  
Chief Cells ◽  
Isolated Gastric Glands ◽  
Pepsinogen Secretion ◽  
Calcium Stimulation ◽  
Intracellular Regulation ◽  
Stimulus Secretion Coupling ◽  
Stimulation Of

Rabbit isolated gastric glands were treated with digitonin so that stimulation of pepsinogen secretion could be studied in a permeable system. Criteria for permeabilization were the release of lactate dehydrogenase in response to digitonin as well as the finding that calcium stimulation and spermine inhibition required the presence of digitonin. Other evidence confirmed that digitonin directly permeabilized chief cells. Pepsinogen secretion was elicited from digitonin-treated gastric glands by a number of agents, including calcium, vanadate, cholecystokinin octapeptide (CCK-OP), 8-bromo-adenosine 3',5'-cyclic monophosphate, and forskolin. Spermine was found to inhibit secretion stimulated by each of these agents only in the presence of digitonin, suggesting an intracellular site of spermine action. We concluded that spermine inhibition of secretion could be used as a marker of secretion elicited from permeable chief cells. The ability to stimulate pepsinogen secretion by such agents as CCK-OP and forskolin suggests that stimulus-secretion coupling is virtually intact even in permeable chief cells. We felt that this preparation should offer unusual opportunities for investigating the mechanisms involved in the intracellular regulation and activation of pepsinogen secretion.

Stimulation of pepsinogen release from isolated gastric glands by cholecystokininlike peptides

1983 ◽  
Vol 244 (2) ◽  
pp. G192-G197 ◽  
Author(s):  
S. J. Hersey ◽  
D. May ◽  
D. Schyberg
Keyword(s):  
Acid Formation ◽  
Weak Base ◽  
Gastric Glands ◽  
Cholecystokinin Octapeptide ◽  
Peptide Receptor ◽  
Isolated Gastric Glands ◽  
Pepsinogen Secretion ◽  
Weak Stimulus ◽  
Peptide Stimulation ◽  
Stimulation Of

Gastric glands isolated from rabbit stomach were employed to study the regulation of pepsinogen secretion by peptide hormones. Cholecystokinin octapeptide (CCK-OP) stimulated pepsinogen secretion with an ED50 of about 1 nM. Caerulein was as effective as CCK-OP but less potent (ED50, 10 nM). Gastrin (HG-17) was found to be a weak stimulus, being only about 20% as effective as CCK-OP or caerulein. Sulfation of CCK-OP and caerulein was found to be important for potency but did not alter efficacy. Peptide stimulation of pepsinogen secretion was unaffected by cimetidine, atropine, or propranolol. Combinations of peptides resulted in less-than-additive responses, as did the combination of peptides with carbachol. In contrast, combination of peptides with isoproterenol resulted in additive responses. Accumulation of the weak base aminopyrine was used to measure acid formation by the gastric glands. The peptides gastrin, CCK-OP, and caerulein were found to be equally effective in stimulating acid formation. The peptide stimulation of pepsinogen secretion was inhibited by dibutyryl cGMP, whereas stimulation of acid formation was not inhibited by the cyclic nucleotide. The results indicate that gastric glands contain at least two peptide receptors distinguishable by sensitivity to dibutyryl cGMP. The peptide receptor associated with pepsinogen secretion appears to be selective for CCK relative to gastrin.

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

Follicle-stimulating hormone-dependent estrogen secretion by rat Sertoli cells in vitro: Modulation by calcium

1991 ◽  
Vol 125 (3) ◽  
pp. 280-285 ◽  
Author(s):  
J. Alan Talbot ◽  
Ann Lambert ◽  
Robert Mitchell ◽  
Marek Grabinski ◽  
David C. Anderson ◽  
...  
Keyword(s):  
Sertoli Cells ◽  
Culture Medium ◽  
Follicle Stimulating Hormone ◽  
Dibutyryl Camp ◽  
Immature Rat ◽  
Estradiol Secretion ◽  
Old Rats ◽  
Stimulating Hormone

Abstract We have investigated the role of Ca2+ in the control of FSH-induced estradiol secretion by Sertoli cells isolated from 8-10 days old rats. Exogenous Ca2+ (4-8 mmol/1) inhibited FSH-stimulated E2 secretion such that, with 8 mmol/l Ca2+ and FSH (8 IU/l) E2 secretion decreased from 2091±322 to 1480±84 pmol/l (p<0.002), whilst chelation of Ca2+ in the culture medium with EGTA (3 mmol/l) increased E2 secretion from 360±45 to 1242±133 pmol/l) in the absence of FSH. Further, EGTA (3 mmol/l) markedly potentiated FSH (8 IU/l), forskolin (1 μmol/l) and dibutyryl cAMP (1 mmol/l)-stimulated E2 secretion. Addition of the Ca2+ ionophores, ionomycin (2-5 μmol/l) and A23187 (2 μmol/l), inhibited FSH (8 IU/l)-stimulated E2 secretion by >80%. The effect of ionomycin was totally reversible, whereas that of A23187 was irreversible. Ionomycin (5 μmol/l) had no effect on EGTA-induced E2 secretion in the absence of FSH, but reduced EGTA-provoked E2 secretion by 59% in the presence of FSH (8 IU/l). Similarly, forskolin- and dibutyryl cAMP-provoked E2 production was inhibited 46-50% by ionomycin (5 μmol/l). We conclude that FSH-induced E2 secretion from immature rat Sertoli cells is modulated by intra- and extracellular Ca2+.

Effect of prenatal isoxsuprine on pulmonary oxygen toxicity in the newborn rat

1980 ◽  
Vol 48 (3) ◽  
pp. 505-510 ◽  
Author(s):  
L. Frank ◽  
J. Summerville ◽  
D. Massaro
Keyword(s):  
Enzyme Activities ◽  
Oxygen Toxicity ◽  
Fetal Lung ◽  
Antioxidant Enzyme Activities ◽  
Newborn Rats ◽  
Lung Maturation ◽  
Lung Weight ◽  
Pregnant Rats ◽  
Rat Pups ◽  
Hyperoxic Exposure

Isoxsuprine, a beta-sympathomimetic agent used clinically to delay premature parturition and to possibly accelerate fetal lung maturation, was administered to pregnant rats at 48 and 24 h prior to delivery. Newborn rats were placed in 96-98% O2 (or room air) to determine if the prenatal isoxsuprine treatment compromised their tolerance to prolonged hyperoxic exposure. (Exogenous catecholamines are known to exacerbate O2 toxicity in adult animals). Survival of the isoxsuprine-treated pups in O2 (52%) was no different than for control neonates exposed to hyperoxia for 7 days (57%) (P = 0.22). Body weight, lung weight, lung protein, and DNA content of the newborns were also not altered by the prenatal isoxsuprine treatment. Lung antioxidant enzyme activities for superoxide dismutase, catalase, and glutathione peroxidase were the same at birth in the isoxsuprine-treated and control rat pups, and the enzyme activities increased in response to hyperoxic exposure in each group to an equivalent degree. Thus, in utero treatment with isoxsuprine had no apparent adverse effect on newborn rats exposed to a prolonged O2 challenge.

THE ROLE OF THE MOTHER IN 131I METABOLISM OF SUCKING AND WEANLING RATS

1965 ◽  
Vol 43 (3) ◽  
pp. 431-436 ◽  
Author(s):  
M. Samel ◽  
A. Caputa
Keyword(s):  
Urinary Bladder ◽  
In Utero ◽  
The State ◽  
Newborn Rats ◽  
Weanling Rats ◽  
Immature Rats ◽  
Other Substances ◽  
Old Rats

In newborn rats the mother provokes the emptying of the urinary bladder by stimulating the perineum with her tongue. The possibility that mothers may thereby ingest the urine of their young has been studied by means of 131I on nine litters of rats aged 10 to 29 days. The results indicate that a considerable quantity of 131I administered intraperitoneally to 10- and 18-day-old rats, which were then reunited with their mothers for 4 hours, reappears in the organism of uninjected nurslings after passing through the organism of the mother. The amount of 131I transferred from injected rats into the bodies of isolated uninjected rats of the same litter decreased during the period of weaning. The observed recirculation of 131I between immature rats and their mothers in both directions may represent a saving mechanism which might include several other substances and would compensate for their loss via the milk, and suggests a new aspect of maternal–neonatal interrelationship which appears as a continuation of the state existing in utero.

Plasma constituents and mortality in rat pups given chronic insulin via injection, pellet, or osmotic minipump

2002 ◽  
Vol 80 (3) ◽  
pp. 180-192 ◽  
Author(s):  
Carl I Thompson ◽  
John W Munford ◽  
Edward H Buell ◽  
Robert J Karry ◽  
Charles T Lee ◽  
...  
Keyword(s):  
Age Differences ◽  
Plasma Glucose ◽  
Rapid Development ◽  
Daily Injection ◽  
Subcutaneous Insulin ◽  
Insulin Administration ◽  
Osmotic Minipump ◽  
Plasma Triglycerides ◽  
Rat Pups ◽  
Old Rats

Two studies compared the glucose responses of 9-day-old rats given subcutaneous insulin, either continuously or via daily injection, for 10 days. In Experiment 1, implanted pellets released a total of 0, 1.9, or 5.7 U insulin/kg the first 24 h. Injected doses were larger, 0 or 8 U/kg. Injections caused no deaths, but insulin-releasing pellets caused high mortality within 24 h. Pups surviving the pellets were normoglycemic by treatment day 8. In Experiment 2, pups received 0.184 U of insulin daily, approximately 8 U/kg at 9 days, via either injection or osmotic minipump. All pups survived. Injected pups were hypoglycemic 2 h postinjection through treatment day 10, whereas pups with insulin minipumps were normoglycemic by day 5. Insulin injections, but not minipumps, lowered plasma triglycerides on day 10. To examine age differences in response to insulin, additional pups and adults received daily injections of 0 or 8 U/kg for 10 days. All survived. Insulin lowered plasma glucose more in pups than in adults and reduced triglycerides in pups but not in adults. The rapid development of normoglycemia in pups with insulin minipumps, compared with pups injected daily with the same dose, suggests that continuous early insulin may produce insulin resistance.Key words: route of insulin administration, insulin resistance, mortality, plasma glucose, development.

Peculiarities of the ultrastructure of neurons of the neocortex of 5-day-day rats under conditions of prenatal alcoholization

2021 ◽  
Vol 23 (1) ◽  
pp. 35-38
Author(s):  
L. I. Bon ◽  
◽  
S. M. Zimatkin ◽  
Keyword(s):  
Oxidative Stress ◽  
Pyramidal Neurons ◽  
Direct Action ◽  
Ultrastructural Changes ◽  
Initial Weight ◽  
Rat Pups ◽  
White Rats ◽  
Old Rats ◽  
Antenatal Alcoholization

The aim of this work was to study the ultrastructure of the internal pyramidal neurons of the neocortex of 5-day-old rat pups after antenatal alcoholization. The studies were carried out on female outbred white rats with an initial weight of 230 ± 20 g and their offspring. Prenatal alcoholization causes deep and varied ultrastructural changes in pyramidal neurons in the neocortex of 5-day-old rats. Moreover, these violations of direct action not only as a consequence of the damaging effect of alcohol, its metabolite acetehyde or the oxidative stress they cause on the membranes and organelles of neurons during embryogenesis, but also as a violation of the normal "program" of development" of neurons in the cortex.

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