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Biomedical subjects

A Guidotti

Publications and source records attributed to A Guidotti.

At least 325 records · Page 18Linked to original sources
PubMed1973

Involvement of adenosine 3',5'-monophosphate in the activation of tyrosine hydroxylase elicited by drugs.

Immediately after the injection of reserpine (16 micromoles per kilogram, intraperitoneally), aminophylline (200 micromoles per kilogram, intraperitoneally), and carbamylcholine (8.2 micromoles per kilogram, intraperitoneally), the concentration of adenosine 3',5'-monophosphate in adrenal medulla of rats is increased severalfold. The three drugs also cause a delayed increase of medullary tyrosine hydroxylase activity. Our results are consistent with the view that an increase of medullary adenosine 3',5'-monophosphate concentration is involved in the drug-induced increase of tyrosine hydroxylase activity in adrenal medulla. Experiments with tyramine (130 micromoles per kilogram, intraperitoneally) suggest that the increase of tyrosine hydroxylase activity and of adenosine 3',5'-monophosphate concentrations is independent of an increase in adrenal catecholamine turnover rate.

Adrenal Medulla↗
PubMed1966

The influences of andrenotropic drugs and noradrenaline on the histamine release in cardiac anaphylaxis in vitro.

1. The regional distribution (auricles, ventricles and septum) of histamine and its release during anaphylaxis were studied in isolated perfused guinea-pig hearts.2. The highest value of histamine content was found in the right auricle, the lowest in the left ventricle and septum, both in normal hearts, and in the hearts subjected to anaphylaxis.3. The fraction of the total histamine released in the course of 24 min by antigen was 50%. The fraction released from the different regions of the heart was similar. No evidence was found for release of 5-hydroxytryptamine.4. A relation was found between the distribution of mast cells and the tissue concentration of histamine. The highest number of mast cells per unit area was found in the right auricle; the lowest in the left ventricle.5. The histamine release by antigen was reduced by previous treatment with (+)-tubocurarine; the histamine release by (+)-tubocurarine was depressed by previous challenge of the heart with antigen.6. Reserpine reduces histamine release. Perfusion of reserpine-treated hearts with noradrenaline partially restored histamine release.7. beta-Adrenergic blocking agents (dichloroisoproterenol and pronethalol) reduced histamine release.8. The drugs tested did not modify the tissue concentration of histamine.9. The possibility of a modulating activity of catecholamines on histamine release in cardiac anaphylaxis is discussed.

Anaphylaxis↗
PubMedDate not supplied

The regulation of hippocampal nicotinic acetylcholine receptors (nAChRs) after a protracted treatment with selective or nonselective nAChR agonists.

In rats, 1 mg/kg twice daily for 10 d of nicotine, a nonselective agonist of nicotinic acetylcholine receptors (nAChRs), fails to change alpha4 and beta2 nAChR subunit mRNA but significantly decreased alpha7 nAChR subunit mRNA and protein expression, which is associated with a 35-40% decrease in the number of 125I-alpha-Bgtx binding sites in hippocampus. In addition, this schedule of nicotine treatment produced a 40% increase in the number of high- (K(D) 1 nM), but decreased by 25% the number of low-affinity (K(D) 30 nM) binding sites for 3H-epibatidine in hippocampus. In contrast, repeated treatment with lobeline (2.7 mg/kg twice daily for 10 d), which selectively binds to high-affinity binding nAChRs, fails to change the expression of high- or low-affinity nAChRs. These data suggest that a simultaneous upregulation of high-affinity nAChRs and downregulation of low-affinity nAChRs is elicited by ligands that can bind to both low- and high-affinity nAChRs, but not by selective agonists of high-affinity nAChRs. One might infer that in hippocampus, high- and low-affinity nAChRs may be located in the same cells. When these two receptor types are stimulated simultaneously by nonselective ligands for high- and low-affinity nAChRs, they interact, bringing about an increase in binding site density of the high-affinity nAChRs.

Animals↗
PubMedDate not supplied

Modulation of phospholipases A2 and C activities against dilauroylphosphorylcholine in mixed monolayers with semisynthetic derivatives of ganglioside and sphingosine.

Most of the semisynthetic ganglioside and sphingosine derivatives studied here decreased the rate as well as the extent of hydrolysis of monomolecular layers of dilauroylphosphorylcholine (dlPC) by both phospholipase A2 (PLA2) and C (PLC). For PLA2, the rate of enzymatic activity was inversely correlated (p < 0.001) with the duration of the latency period of the enzymatic reaction. The correlation between the rate of activity and the latency period was not statistically significant for PLC. The potency to inhibit PLA2 and PLC was not significantly correlated with the presence of specific chemical groups. Also, the inhibitory effect is not correlated to changes of the substrate intermolecular spacing or surface potential caused by the sphingolipids (SLs). Conversely, for PLA2 the variation of the kinetic parameters of the reaction with the molecular polarization vector of the SLs are statistically significant (p < 0.01). The rate of phospholipid degradation by PLA2 decreased, and the lag times tended to become longer, with increasing values of the SLs' polarization vector. The kinetic parameters of the reaction with PLC did not show statistically significant correlation with the polarization vector of the SLs. Our results suggest that the configuration of the electrostatic field across the interface is more important than are formal charges or specific chemical moieties in modulating the activity of PLA2. Inhibition of phospholipase activities of these types by specific SLs or their metabolites may be important as supramolecular regulatory steps at the membrane level of the amplification of lipid-mediated signaling pathways.

Carbohydrate Sequence↗