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Biomedical subjects

M C Ruiz

Publications and source records attributed to M C Ruiz.

At least 55 records · Page 3Linked to original sources
PubMed1991

Rotavirus infection alters Na+ and K+ homeostasis in MA-104 cells.

Infection of MA-104 cells with the OSU strain of rotavirus induced an increase in Na+ and a decrease in K+ intracellular concentrations, starting at 4 h post-infection. These changes were not related to an inhibition of the Na+/K+ pump since ouabain-sensitive 86Rb uptake was augmented in rotavirus-infected cells compared to control cells, whereas the [3H]ouabain binding and Na+/K+ ATPase activity in the cell homogenate were unaffected. Furosemide-sensitive 86Rb uptake (Na+/K+/2Cl- cotransport) was not modified by the infection. Passive 86Rb efflux and 22Na influx were augmented in infected cells suggesting an increase in the plasma membrane permeability. The increase in intracellular Na+ concentration might be responsible for the observed stimulation of the Na+/K+ pump. This effect was dependent upon the synthesis of viral proteins because it was abolished by addition of cycloheximide up to 4 h post-infection. Prevention of the increase in intracellular Na+ by the use of low Na(+)-containing media did not modify the pattern of protein synthesis. This suggests that changes in intracellular Na+ and K+ concentrations were not related to shutoff of cellular protein synthesis. Alterations of ion contents in the rotavirus-infected enterocytes might impair intestinal absorptive capacity before the appearance of histopathological lesions.

Animals↗
PubMed1990

Increased calcium permeability is not responsible for the rapid lethal effects of amphotericin B on Leishmania sp.

The mode of action of the polyene antibiotic amphotericin B (AmB), the drug of choice for the treatment of systemic fungal infections and visceral leishmaniasis, is still unclear. An increase in intracellular Ca2+ concentration [( Ca2+]i), toxic in many cases, has been postulated as a possible lethal mechanism for AmB. Cell permeabilization to ethidium bromide (EB) was used as a criterion of viability. Kinetics of the DNA-EB fluorescent complex formation was studied in ergosterol-containing Leishmania promastigotes. Intracellular Ca2+ concentration was measured using quin-2 fluorescence in parallel aliquots. It is shown in this work that AmB can act as an efficient Ca2+ ionophore. However, the rapid permeabilization effect induced by AmB on these cells was not dependent on an increase in [Ca2+]i. On the contrary, it was found that leishmanicidal effect of AmB was enhanced in the absence of external calcium. Furthermore, A23187 a Ca2+ ionophore did not provoke cell permeabilization to EB.

Amphotericin B↗
PubMed1989

Role of Ca2+ in H+ transport by rabbit gastric glands studied with A23187 and BAPTA, an incorporated Ca2+ chelator.

The role of Ca2+ in stimulation of H+ gastric secretion by cAMP-dependent and -independent secretagogues was studied in isolated rabbit glands using Ca2+ ionophore, A23187, and an intracellular Ca2+ chelator (BAPTA, 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid) incorporated as its acetoxymethyl ester (BAPTA-AM). Acetylcholine (ACh), tetragastrin (TG), histamine and forskolin induced a transitory increase of intracellular Ca2+ concentration, [Ca2+]i, measured in gastric glands loaded with Ca2+-sensitive dye fura-2, and provoked an acid secretory response evaluated with aminopyrine accumulation ratio (AP ratio). The Ca2+-ionophore A23187 also induced an increase in [Ca2+]i and in AP ratio. cAMP-dependent secretagogues were more potent stimulants of acid secretion than cAMP-independent secretagogues. cAMP analogue, 8-bromo-adenosine 3',5'-cyclic monophosphate (8-BR-cAMP) induced an increase in AP ratio without modifying [Ca2+]i. BAPTA-AM (5-25 microM) induced a transient decrease of resting [Ca2+]i which returned to basal level due to extracellular Ca2+ entry. Increases in [Ca2+]i produced by ACh and TG were abolished by BAPTA and those produced by Ca2+ ionophore A23187 were partially buffered. BAPTA inhibited in a dose-dependent manner H+ secretion induced by cholinergic and gastrinergic stimulants in the presence of cimetidine. A23187 increased the AP ratio to values similar to those obtained with ACh or TG and was not inhibited by BAPTA. BAPTA partially inhibited (40%) the increase in AP ratio induced by forskolin and histamine inspite of the complete inhibition of the Ca2+ response. BAPTA did not inhibit the response to 8-BR-cAMP. BAPTA inhibition of forskolin stimulation was reversed by A23187 and the response was potentiated. These results indicate that ACh and TG response are completely dependent on an increase of [Ca2+]i. The response to cAMP-dependent agonists histamine and forskolin depend both on Ca2+ and cAMP. For forskolin stimulation the response may be the result of a potentiation between Ca2+ and cAMP.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1988

Mammalian-like differentiation of gastric cells in the shark Hexanchus griseus.

Gastric glands of submammalian vertebrates are formed by one single cell type known as the oxyntopeptic cell. This cell secretes both hydrochloric acid and pepsinogen. In mammals, this cell differentiates into an acid secreting cell and a pepsinogen secreting one. In the elasmobranch fish Hexanchus griseus we observed, by means of histological studies at the light- and electron-microscopic levels, two different cell types for the secretion of acid and zymogen. This organization represents an evolutionary divergence in a primitive animal, i.e., the appearance of a feature that is acquired much later in evolution, in mammals.

Animals↗
PubMed1988

Somatostatin inhibition of secretagogue and forskolin-stimulated gastric acid secretion.

The action of somatostatin (SS) on acid secretion and histamine release was studied in isolated gastric mucosa of toads mounted in Ussing chambers. SS inhibited H+ secretion and histamine release stimulated by cholinergic and gastrinergic secretagogues. Exogenous histamine stimulation of H+ secretion was blocked noncompetitively by SS in a dose-dependent manner. In mucosae maximally stimulated by histamine or forskolin and cimetidine, acetylcholine (ACh) and tetragastrin (TG) induced a direct stimulation of the oxyntopeptic cell not inhibited by SS. Indomethacin, an inhibitor of prostaglandin synthesis, did not prevent SS inhibition of histamine stimulation. Pretreatment with SS abolished forskolin stimulation of H+ secretion. SS induced a small inhibition of the stimulatory effect of N6, 2'-O-dibutyryladenosine 3',5'-cyclic monophosphate. These results suggest that SS inhibits acid secretion stimulated by secretagogues through different mechanisms: 1) inhibition of histamine release by ACh and TG, 2) inhibition of endogenous and exogenous histamine stimulation through a blockade of adenylate cyclase, and 3) an inhibitory effect subsequent to the synthesis of adenosine 3',5'-cyclic monophosphate. The direct activation of the oxyntopeptic cell by ACh and TG does not seem to be affected by somatostatin.

Acetylcholine↗
PubMed1987

Ultrastructural studies of endocrine-like cells in the fundic gastric mucosa of the bullfrog, Rana catesbeiana.

This study is concerned with electron-microscopic observations on endocrine or paracrine cells in the fundic gastric mucosa of the bullfrog. Also, an attempt was made to identify the histamine-releasing cells involved in the secretagogue response. At least three distinct endocrine-like cell types were found. The classification is based on the appearance of secretory granules and other organelles, and the relationship of endocrine-like cells with other cells in the tissue. The amphibian endocrine-like cells resemble the ECL, D and EC cells of mammals. Type-I (ECL) cells showed degranulation after repeated stimulation with tetragastrin (TG), acetylcholine (ACh) and K+ depolarizing solution, all of which release histamine.

Acetylcholine↗
PubMed1986

Stimulation of oxyntic and histaminergic cells in gastric mucosa by gastrin C-terminal tetrapeptide.

Gastrin tetrapeptide (TG) stimulation of H+ secretion and histamine release and their relationship were characterized in isolated amphibian gastric mucosa. TG released histamine and stimulated H+ secretion. Dose-response curves to TG showed nonparallel increases in both parameters. In tachyphylaxis experiments, there was no correlation between histamine release and H+ secretion. Comparison of cimetidine inhibitory dose-response curves of maximal TG or histamine stimulation showed a much higher sensitivity for TG-stimulated H+ secretion. This suggests that the pericellular histamine concentration released by TG was lower than that needed for maximal response. In mucosae maximally stimulated by histamine, TG induced a further increase in H+ secretion. In the presence of cimetidine, there was potentiation between TG and dibutyryl cAMP that was dependent on the presence of extracellular calcium. The results are interpreted to indicate that TG (or gastrin) stimulates H+ secretion through different mechanisms: 1) direct stimulation of the oxyntic cell dependent on extracellular calcium, 2) potentiation between gastrin and histamine, and 3) release of histamine from paracrine cells. Direct stimulation of the oxyntic cell by TG is not sufficient to trigger H+ secretion. Potentiation between TG and histamine at the oxyntic cell may result from interaction between TG-induced increases in intracellular Ca2+ and histamine-induced increases in intracellular cAMP.

Animals↗
PubMed1984

Evidence for a direct action of acetylcholine on the gastric oxyntic cell of the amphibian.

The possibility of a direct action of acetylcholine (ACh) on the oxyntic cell not mediated by histamine release was studied in resting isolated gastric mucosae. H+ secretion and histamine release, and their relationship, were studied under ACh stimulation and other conditions. ACh released histamine from mucosal stores and stimulated H+ secretion. H2-receptor blocker cimetidine largely inhibited ACh-induced stimulation of H+ transport but not histamine release. Atropine inhibited the cholinergic response in both histamine release and H+ secretion. The dose-response curves to ACh showed nonparallel increases in H+ secretion and histamine release. When dose-response curves to exogenous and endogenous histamine (released by ACh) were compared, it was found that ACh increased Vmax for endogenous histamine. Comparison of the effects of ACh with other experimental conditions such as tetragastrin treatment, K+ depolarization, or Na+-free nutrient solution showed that the amount of histamine released by ACh was insufficient to explain the observed rates of secretion. Stimulation by ACh was faster, greater, and more transitory compared with that by histamine. In mucosae maximally stimulated by histamine, ACh induced a further increase in H+ secretion. In the presence of cimetidine, potentiation between ACh and dibutyryl cAMP or isobutyl-methylxanthine was found. The results are consistent with ACh having a dual action on oxyntic and histamine-releasing cells. The action of ACh on the oxyntic cell would potentiate the effect of released histamine. It is suggested that ACh and released histamine act on the oxyntic cell through different second messengers, resulting in the potentiated response.

1-Methyl-3-isobutylxanthine↗
PubMed1983

On the mechanism of stimulation of H+ transport in gastric mucosa by Ca++ ionophore A23187. I. Pathways for cytosolic calcium increase.

The pathways for cytosolic Ca++ increase under A23187 stimulation of H+ secretion were studied in the isolated gastric mucosa of the toad Bufo marinus. A23187 produced a more potent stimulation of secretion when added to the mucosal side which did not contain calcium. Measurements of ionophore incorporation by fluorometric methods indicated that A23187 incorporates into oxyntic cells intracellularly. The presence of divalent cations inhibited incorporation. This may be the reason for a more potent action when A23187 was added from the mucosal side. Withdrawal of calcium from serosal solution largely inhibited the secretory response to A23187 added to the mucosal side. Reintroduction of calcium into the serosal side in the presence of ionophore elicited H+ secretion. The results are consistent with an uptake of A23187 from the mucosal side into cellular organelles and basolateral membranes. Calcium entry through the serosal side may be responsible for triggering secretion. Although A23187 likely releases calcium from intracellular stores, its rate of release may not be sufficient to bring about a full stimulation of secretion in serosal-Ca++-free conditions.

Animals↗
PubMed1983

On the mechanism of stimulation of H+ transport in gastric mucosa by Ca++ ionophore A23187. II. Ca++-cyclic AMP interactions.

The possibility of interactions between calcium and cyclic AMP (cAMP) in the mechanism of stimulation of H+ transport by A23187 was studied in the isolated gastric mucosa of the toad Bufo marinus. A23187 stimulated H+ secretion and histamine release. The amount of histamine released by A23187 did not explain the degree of stimulation. Metiamide partially inhibited the response to A23187. Ca++ ionophore produced an overstimulation of secretion after H+ transport had been induced by supramaximal effective concentrations of histamine (10-4 M). In the presence of metiamide, IMX potentiated the response to A23187. Also, in the same condition (metiamide treated) the effects of db-cAMP and A23187 were additive. The results are consistent with an interaction between Ca++ and ionophore-released histamine at the oxyntic cell in the stimulation by A23187. The stimulatory response may be the result of a potentiation between calcium and cAMP at the intracellular level.

Animals↗
PubMed1980

[Attempted interpretation of water injected into the inguinal artery on the augmentation of intramammary pressure of the sheep].

The increase in intramammary pressure caused by injecting small amounts of water into the udder artery of anesthetized ewes does not seem to be a nervous reaction induced by the stimulation of sensitive mammary receptors: the deflections remain unchanged after complete denervation of the gland (fig. 4) and after the injection of water at different temperatures (4 to 37 degrees C; fig. 1) or pH's (4.6 to 9.8; fig. 2). Since injecting the same volumes of blood (fig. 3), isotonic NaCl (fig. 5) or glucose (fig. 6) solutions does not cause the intramammary pressure to increase, water effect would appear to result from a change in blood osmotic pressure. Among the substances released when the blood corpuscles or platelets are destroyed, kallikrein and histamine do not seem to play a role. These products induce intramammary pressure to rise (fig. 7, 9) but latency and duration are longer than with water Also, their respective inhibitors, aprotinin and phenergan, always block their effect on intramammary pressure but not that of water. On the other hand, water and bradykinin (fig. 8) produce similar responses, indicating that the latter substance may play a role. We must consider also the possible action of extra-capillary water transfer, modifying ion flux and myoepithelial cell membrane potential or simply inducing the alveolar cells to swell and the acini to flatten. This last hypothesis permits a better interpretation of the pressure decreases noted after injection of hypertonic solutions (figs. 5, 6) since reverse water movements would have the opposite effect.

Animals↗
PubMed1976

[Hydrolytic conditions of the conjugated steroids from human urine (author's transl)].

The hydrolisis of dehydroepiandrosterone sulfate added to human urine was studied under several hydrolytic procedures. Enzymatic and acid hydrolysis with and without the previous removal of enzymic inhibitors present in the human urine were compared. The simple precipitation of inorganic ions with barium acetate before the enzymatic hydrolysis was considered an efficient procedure giving an 81% recovery of the added dehydroepiandrosterone. Since this procedure does not involve rearrangements in the steroid molecules, and because of its simplicity it is considered adequate for the determination of the urinary steroid excretion patterns in humans allowing the quantitation of some conjugates (16 alpha-hydroxy-dehydroepiandrosterone) otherwise not detectable because of its incomplete hydrolysis and extraction.

17-Ketosteroids↗
PubMed1975

[Free amino acids in the amniotic fluid and in maternal blood in advanced pregnancy].

We have studied a series of sixteen free amino-acids as well as total blood amino-acid and liquor amino-acids in 56 women between the 25th and 44th weeks of pregnancy. The results have been analysed statistically and demonstrated graphically. The amino-acid levels rise from the 25th week of the pregnancy until term (p less than 0.05) in peripheral blood. On the other hand the total level of amino-acids in the amniotic fluid drops from the 25th week of pregnancy remarkably (p less than 0,01). Different amino-acids show different curves. The increase in the level of total blood amino-acids is principally due to a rise in glycine and leucine, while the other amino-acids as a whole stay constant. The spectrum of amino-acids in the amniotic fluid is however a little different and the drop in total amino-acids if principally due to the threonine-serine fraction and partly to the glutamine, proline, alanine, lysine and valine elements, whereas the rest stay the same or even raised.

Alanine↗