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Biomedical subjects

L M Botana

Publications and source records attributed to L M Botana.

88 records · Page 5Linked to original sources
PubMed1991

[Effect of isoproterenol on the liberation of histamine from rat lung mast cells].

Rat lung mast cells were stimulated with drugs with distinct mechanisms of action, namely concanavalin A, compound 48/80 ionophore A23187, in the presence of the beta adrenergic agonist (-)isoproterenol. Cells show a high response when they are stimulated with FNa-calcium. Isoproterenol does not inhibit histamine release induced by any stimuli, but enhances the response to concanavalin A and compound 48/80. Results point to the lack of beta activity on rat lung mast cells.

Animals↗
PubMed1991

[Inhibition of histamine liberation in mast cells from the lung and the intestine of the dog by isoproterenol].

Enzymatically isolated dog lung and gut mast cells were stimulated with compound 48/80, ionophore A23187, concanavalin A and FNa-Ca. Cell response elicited by A23187, concanavalin A or 48/80 is almost completely inhibited by isoproterenol. Concanavalin A induced histamine release on gut mast cells is high, indicating an elevated degree of sensitization of these cells. Results point to the existence of beta adrenergic inhibitory activity on dog lung and gut mast cells.

Animals↗
PubMed1988

Somatostatin structure-activity studies in the stomach.

Somatostatin may inhibit gastric exocrine functions independent of blockade of gastrin secretion. In order to further investigate this suppressive effect, somatostatin derivatives were injected to cats bearing a cannulated gastric fistula under pentagastrin stimulation. Results showed that somatostatin-14 was more potent than somatostatin-28 in this particular model. Analogues with substituted residues exhibited a variable spectrum of actions on hormone release and gastric function. A cyclic pentapeptide was deprived of gastric or GH inhibitory properties whereas the related peptide with a benzyl-protecting group on Thr was only devoid of gastric effect. The octapeptide SMS 201-995 was described as a potent inhibitor of gastric secretion in comparison with natural somatostatin in rats and also in humans, but was unable to induce maximal suppression of acid output in the cat model. Differences in gastric effect of different derivatives could be explained on the basis of binding to a selective subset of receptors, since at least two binding sites have been identified in the stomach mucosa. Serial studies with short cyclic somatostatin should help to establish a clear relationship between peptide structure and inhibition of gastric secretion.

Animals↗
PubMed1987

Adrenergic agonists do not compete with the antagonist (-)3-[125I]iodocyanopindolol for binding to rat pleural or peritoneal mast cell adrenergic receptor.

(-)3-[125I]iodocyanopindolol (ICYP), a high selective, high specific beta antagonist is employed to characterize beta-adrenoceptors on rat pleural and peritoneal mast cell populations. Results show that non specific binding is low, and that pleural mast cells exhibit greater number of receptors per cell (140,000) than peritoneal cells (90,000). Dissociation constants (Kd) are 0.37 +/- 0.01 and 0.55 +/- 0.02 nM for pleural and peritoneal cells, respectively. Competition experiments show that isoproterenol do not displaces ICYP neither in pleural nor in peritoneal cells. Low concentrations of propranolol displace ICYP from its binding sites, but atenolol does not. Results point to the existence in mast cells of mainly atypical. beta 2-receptors, since the agonist isoproterenol does not compete with the antagonist ICYP.

Adrenergic alpha-Agonists↗
PubMed1987

Adrenergic activity on rat pleural and peritoneal mast cells. Loss of beta-receptors during the purification procedure.

Adrenergic agonists inhibit the release of histamine from rat pleural and peritoneal mast cells stimulated with compound 48/80 to a degree dependent on their beta-activity. Isoprenaline takes part in a stereoselective inhibitory action in the range 10(-7)-10(-4) M. Adrenaline induces a similar response pattern, with inhibition at higher concentrations. The response profile, but not the maximum values of inhibition, is clearly dependent on the concentration of the histamine releaser. Noradrenaline by itself is a histamine releaser, no stereoselectivity being observed. In the presence of compound 48/80 it takes part in a non-stereoselective inhibitory reaction at low concentrations. Inhibition of histamine release by isoprenaline was antagonized by 10 or 100 microM propranolol except at the highest isoprenaline concentration (1 mM). Both atenolol and propranolol nullified the inhibitory activity of noradrenaline, but not the increased histamine release it induces at higher concentrations (at least when acting in conjunction with compound 48/80). When rat mast cells are purified through Percoll, a change in their response profiles is observed. Isoprenaline and adrenaline by themselves elicit non-specific release of histamine; with compound 48/80, release is additive in the case of isoprenaline and supra-additive in the case of adrenaline. Results point to the loss of beta-adrenergic inhibitory activity after purification.

Animals↗
PubMed1986

In vivo inhibition of polymyxin B-induced hypotension: evidence of beta-adrenergic inhibitory activity on rat mast cells.

In vitro, rat mast cells show a dose-inhibition profile when stimulated with compound 48/80 in the presence of isoprenaline. Isoprenaline-induced inhibition is stereoselective at low concentrations, being greater on pleural mast cells. In vitro, polymyxin B (0.02-0.05 mg/kg) induces a marked hypotension and slow heart rate, but not tachyphylaxis. Both effects were not suppressed in the presence of isoprenaline (with short half-life in vivo), but orciprenaline does induce a clear inhibition of Polymyxin B-induced hypotension, which correlates well with heart rate.

Animals↗
PubMed1986

[Response of pleural and peritoneal mastocyte populations in the rat to agents with different mechanisms of action].

Histamine release from rat pleural and peritoneal mast cells not previously purified is presented. Cells are stimulated by different mechanism-acting pharmacologic agents. FNa, theophylline, ruthenium red, chlorpromazine and propranolol are used. Results show that both cell populations are pharmacologically different, with distinct responses in the presence of FNa or chlorpromazine. Chlorpromazine and propranolol are cytolytic agents.

Animals↗
PubMed1986

Effect of calcium on histamine release from pleural and peritoneal mast cells induced by catechol.

Histamine release from rat pleural and peritoneal mast cells induced by catechol (1, 10, 50, 250 microM and 1 mM) has been studied. The dose-response induced by catechol is non-cytotoxic, is not modified by purification of mast cells and is calcium independent. The sensitivity and maximum response to catechol is the same irrespective of the presence or absence of Ca++, except on purified pleural mast cells, that showed a plateau response at 250 microM catechol in the absence of Ca++, and on unpurified peritoneal mast cells which exhibited a lower maximum response equally in the absence of Ca++. The release is induced by catechol at concentrations as low as 50 microM in all cases, and the maximum response is reached at 1 mM.

Animals↗
PubMed1986

[Na+ K+ ATPase activity in mast cells from the pleural and peritoneal cavities of the rat].

ATPase activity in rat mast cells was studied, assuming that pleural and peritoneal mast cells are different populations. Mast cells were purified with Percoll. Enzymatic activity was found to be 36% higher in pleural cells that in peritoneal cells. Moreover, for both populations results show a Na+-K+ ATPase activity either low or slightly inhibited by ouabain.

Animals↗
PubMed1985

Difference in, and influence of the purification medium on, sensitivity and maximum response of peritoneal and pleural mast cells stimulated by certain polyamines.

The actions of the polyamines compound 48/80, poly-l-lysine and polymyxin B on rat pleural and peritoneal mast cell secretion have been studied. Unpurified pleural mast cells released more histamine than peritoneal mast cells when stimulated by submaximal concentrations of compound 48/80 and poly-l-lysine, but the same profile of response was observed with polymyxin B in both populations. Dose-response studies of peritoneal and pleural mast cells purified with Percoll and Ficoll and stimulated by polymyxin B showed a decreased sensitivity and decreased maximum response of peritoneal cells when Percoll was used. The maximal response of pleural cells and the sensitivity of peritoneal cells were affected only slightly by Ficoll.

Animals↗
PubMed1984

Milk progesterone radioimmunoassay using radioiodinated tracers: a rapid and reliable assay system.

Both the validity and practicability of a direct progesterone radioimmunoassay based on radioiodinated progesterone tracers were studied. The results obtained show the reliability of the assay; when compared with assays based on 3H-progesterone tracers there are fewer steps for assay execution, saving time and reducing the number of reagents used. Various commercially available 125I-progesterone tracers were assayed, and only those with an 11 alpha-hemisuccinate bridge were suitably bound by antisera raised against progesterone-bovine serum albumin conjugates having identical bridge structure. The bridge effect caused no observable alteration in validity parameters. Finally, our results support the utility of this assay as a practical method of early diagnosis of pregnancy and as a reliable experimental technique to monitor cow ovarian function.

Animals↗
PubMed1983

[Isolation of mastocytes from rat peritoneal fluid using continuous Ficoll gradients].

A method for mast cells purification from rat peritoneal fluid is described. The method consists of a continuous Ficoll gradient between 20 and 22,5% (w/v) Ficoll and the cells are obtained with an 88% retrieval. Purity and viability were of 95% and 97% respectively. The cells so purified were functional against the compound 48/80 and the spontaneous secretion value was less than 8%.

Animals↗
PubMed1983

[Secretory activity of mast cells in the presence of cholinergic agonists].

Mast cells from rat peritoneal fluid were studied under cholinergic stimulus. The cells were purified by a continuous Ficoll gradient and were challenged with acetylcholine and carbamylcholine. The preparations showed the typical dose-response pattern against compound 48/80 with a dose interval of 0.5-1 microM that clearly increased the secretion. However, the histamine release elicited by increasing concentrations of acetylcholine and carbamylcholine was of little magnitude and similar for all the concentrations; this kind of response has not a dose-response profile and does not appear to be explained by the presence of a cholinergic receptor on the mast cell cellular membranes. The cholinergic agents neither stimulated directly the mast cells nor did they cause any variation in the 48/80 response. The histamine release pattern obtained with these agents cannot support the hypothesis of a primary cholinergic receptor on mast cells. However, if such receptor existed, its action could only be of secondary importance, and in fact such action was not manifested with the compound 48/80.

Acetylcholine↗
PubMedDate not supplied

Study of cytoskeletal changes induced by okadaic acid in BE(2)-M17 cells by means of a quantitative fluorimetric microplate assay.

The diarrhogenic activity of the marine toxin okadaic acid (OA) has been associated to its actin-disrupting effect, which could reflect the loosening of tight junctions in vivo. In this report, we present results obtained using a fluorimetric microplate assay for quantitative measurements of OA-induced changes on F-actin pools in BE(2)-M17 cells. The proposed method shows important advantages over classical methods in terms of rapidity, sensitivity (less than 5000 cells per well) and reproducibility, thus providing a very useful tool for studying F-actin levels in living cells. Results obtained demonstrate a time- and dose-dependent decrease of F-actin pools (IC(50)=100 nM at 1 h) in OA-treated cells, which was partly counteracted by TPA, H89, forskolin, wortmannin, ionomycin and orthovanadate at early stages, but remained unaffected after 24 h of incubation. Cells exposed for 1 h to 1 nM OA showed a slight increase of F-actin pools (1.5-fold), which was blocked by genistein and lavendustin A, thus suggesting a role for tyrosine kinases-dependent pathways in OA-induced polymerization at low concentrations. These results suggest direct interactions of Ser/Thr protein phosphatases with actin-binding proteins in the regulation of actin polymerization, thus indicating that disruption of cytoskeletal structure may be a key mechanism of OA-induced diarrhea.

Actins↗