Regulation of intestinal motility by different muscarinic receptor subtypes.
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Biomedical subjects
Publications and source records attributed to S Lecchini.
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Intracellular free calcium concentrations (Ca++i) were studied in polymorphonuclear leukocytes (PMNs) from 13 athyreotic patients who had been previously treated by total thyroidectomy and radioiodine therapy for differentiated thyroid carcinoma, and from age- and sex-matched euthyroid healthy controls. Patients were studied twice, when hypothyroid (visit 1) and after restoration of euthyroidism by L-T4 TSH-suppressive therapy (visit 2). PMNs from patients at visit 1 had significantly lower resting (Ca++)i levels compared to both visit 2 and controls. Values at visit 2 did not differ from those of the controls. Stimulus-induced (Ca++)i rise was also significantly blunted at visit 1 and normalized at visit 2, possibly through a differential contribution of distinct intracellular Ca++ stores, as suggested by the response pattern to the chemotactic agent, N-formyl-Met-Leu-Phe (fMLP), to the selective SERCA pump inhibitor, thapsigargine, and to the mitochondrial uncoupler, carbonyl cyanide p-trifluoromethoxyphenyl-hydrazone (FCCP). In vitro treatment of PMNs from healthy subjects with high TSH concentrations impaired intracellular Ca++ store function. Both resting (Ca++)i levels and fMLP-induced (Ca++)i rise increased in the presence either of low-concentration TSH or of T4, but effects of TSH and T4 were not additive. T3, rT3, and TRIAC had no effect. In conclusion, this study provides evidence for a direct relationship between thyroid status and (Ca++)i homeostasis in human PMNs, mainly related to direct actions of TSH and T4 on these cells.
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Some neuropeptides may influence various functions of immunocompetent cells. Endogenous opioids have been implicated in the correlation of the immune, endocrine and nervous system. The object of our study was to evaluate the effects induced by some agonist and antagonist endogenous peptides to opioid receptors on granulocytes (PMNs) functions in vitro. We used these drugs: D-Ala2-D-Leu6-enkephalin (DADL-Sigma-Chemical-Usa); D-Ala2-N-ME-Phe4-Gly-ol5-enkephalin (DAGO-Sigma-Chemical-Usa); Dynorphin 1-9 (Sigma Chemical-Usa); naloxone (Sigma Chemical-Usa) and morphine (Sifac-Italy). Morphine was able to inhibiting neutrophil granulocyte chemotaxis induced by serum activated with E. Coli (p < 0.01), by casein (p < 0.01 and <fMLP (p < 0.01). Furthermore morphine and 1-9 dynorphin inhibited spontaneous migration of PMNs both when added to the upper compartment together with cells. Naloxone was able to inhibit PMNs chemotaxis induced by serum, casein and fMLP, this drug was not able to behave on chemokinesis or random migration activity. Morphine was found to inhibit PMNs aggregation induced by PHA (0.01), PMA (0.01), fMLP (0.01) and Ca++ ionophore (p < 0.01), ATP release (p < 0.01), thromboxane B2 (TxB2) and leukotriene B4 (LTB4) secretion during cell aggregation. Dynorphin 1-9, per sé, induced TxB2 and LTB4 secretion from PMNs. Morphine inhibition of both cell aggregation and ATP release, but not arachidonic acid metabolism product secretion, was prevented by naloxone. The naloxone sensitive impairment by morphine of CD 11/CD 18 complex surface expression observed could play a role in opioid inhibition of PMNs activation.
BACKGROUND AND OBJECTIVE: Noradrenergic innervation is present in the bone marrow and adrenergic agents can modulate hematopoiesis. However, since no data are available concerning endogenous catecholamines at this level, we investigated their presence and origin. METHODS: Using a high performance liquid chromatographic method, we have and measured endogenous catecholamines in bone marrow from normal, 6-OHDA-treated and pargyline-treated mice. RESULTS: Noradrenaline, adrenaline and dopamine levels were, respectively, 2806.74 +/- 408.85, 803.37 +/- 87.66 and 274.47 +/- 51.54 pg/g of tissue. Noradrenaline levels were lower after 6-OHDA (1130.47 +/- 142.73 pg/g of tissue, p < 0.01 vs. control values) and higher after pargyline (4122.62 +/- 509.54 pg/g of tissue, p < 0.05). None of these treatments significantly affected adrenaline or dopamine content. INTERPRETATION AND CONCLUSIONS: Noradrenaline in the bone marrow originates mainly from sympathetic nerve endings and is metabolized through specific enzymatic pathways. Adrenaline and dopamine may originate from other sources, such as the systemic circulation.