PubMed Health⌕ Search

Biomedical subjects

E Anselmi

Publications and source records attributed to E Anselmi.

At least 37 records · Page 2Linked to original sources

[Influence of endogenous catecholamines on responses of rat lung to beta-adrenergic agonists].

Relaxation responses to the beta-adrenoceptor agonists: isoprenaline (non selective), salbutamol (beta 2-selective) and noradrenaline (plus phentolamine 10(-5) M) (beta 1-selective) have been obtained on rat lung parenchymal strips in the absence and presence of pargyline and tropolone (monoamino-oxidase and catechol-O-methyltransferase inhibitors), cocaine (neuronal uptake blocking agent), corticosterone (extraneuronal uptake inhibitor) as well as in reserpinized rat. Responses to these beta-adrenergic agonists were not potentiated in the presence of any of these inhibitors. This indicates that endogenous catecholamines, enzymatic or uptake processes, do not modulate beta-adrenoceptor mediated responses of rat lung strip and demonstrates that there is no correlation between neuronal uptake/beta 1-adrenoceptors and extraneuronal uptake/beta 2-adrenoceptor mediated responses, as had previously been suggested.

Adrenergic alpha-Agonists↗

A comparison of uterine contraction induced by PGE1 and oxytocin in Ca-free solution.

The contraction of the rat uterus incubated in Ca-free EDTA-containing solution in response to PGE1, oxytocin and vanadate has been investigated in order to examine the mechanism of the release of Ca from intracellular stores. The results obtained show that PGE1 evoked a sustained contraction the magnitude of which diminishes slightly after successive additions of PGE1 but not after long exposure to Ca-free medium. Oxytocin induced two different contractions: one of them was transient and observed only after incubating for 5 min in Ca-free solution; the other remained constant during prolonged incubation in Ca-free medium. Vanadate, an inhibitor of Ca-ATPase, induced sustained contraction after prolonged exposure to Ca-free medium, and isoprenaline, which stimulates Ca re-uptake by intracellular organelles, counteracted the sustained contractile response induced by the three agonists.

Alprostadil↗

Effects of magnesium chloride on the contractile response of uterus to several agonists in Ca-free solution.

The effects of MgCl2 on the oestrogen-dominated rat uterus have been examined. Tissues were preincubated in a Ca2+- and Mg2+-free medium containing 3 mM EDTA. Most experiments were subsequently performed in a similar medium containing either no EDTA or EDTA (1 mM). When MgCl2 was added cumulatively (1-32 mM) no contractile responses were obtained in Ca,Mg-free medium or in Ca,Mg-free high K+ solution. When 2 mM CaCl2 was added, a sustained contraction was obtained. Subsequent addition of cumulative concentrations of MgCl2 caused concentration-dependent relaxation. Oxytocin, 2 microM, produced a small and sustained contraction in a Ca,Mg-free medium. Addition of MgCl2, 2 mM, increased this contraction. In a Ca,Mg-free medium vanadate (8 X 10(-5)M) did not evoke spasm of uterine smooth muscle. After addition of MgCl2 in cumulative amounts (1-32 mM) in the presence of vanadate, a concentration-dependent contraction was obtained. The present work shows that in Ca-free solution, maintained contractions induced by oxytocin and vanadate are augmented by Mg2+.

Animals↗

Effect of PGE2 on sulfonylurea induced insulin release.

1. Previous studies have demonstrated that the administration of prostaglandins (PGs) inhibits insulin secretion in vivo and have suggested that these compounds may be involved in the pathogenesis of diabetes mellitus. The present study was carried out in order to explore the effect of PGE2 on sulfonylurea-induced insulin release. 2. We determined glycemia and insulinemia in rat blood samples, at different times before and after the intraarterial administration of: (a) glibenclamide, (b) tolbutamide, (c) PGE2, (d) glibenclamide and PGE2, (e) tolbutamide and PGE2; in all cases with and without a glucose pulse. (Glibenclamide 0.5 mg/kg, tolbutamide 50 mg/kg, PGE2 100 micrograms/kg and glucose 500 mg/kg). 3. The results of these experiments demonstrate that PGE2 partially inhibits sulfonylurea-induced insulin release. The plasma insulin and glucose levels remain within the range of intermediate values as compared to the control groups (sulfonylurea or PGE2-treated rats) both in presence and absence of glucose.

Animals↗

Role of stored Ca in contractions of rat uterus induced by acetylcholine: effects of preincubation with Mg-free solution.

We have investigated the action of acetylcholine on the release of Ca ions from intracellular stores. The results obtained show that in Ca-free solution acetylcholine induces two different contractions. One of them is a transient contraction that was observed after loading for 5 min in Ca(-) or Ca,Mg(-) solution and its magnitude was not modified by the absence of Mg. Another contraction remains constant after long exposure to Ca(-) medium but decreases in Ca,Mg(-) solution thus indicating that Mg ions are related to it. These results suggest that Mg plays an interesting role in stimulus-contraction coupling mediated by acetylcholine in Ca-free medium. This action can be explained by a release of stored Ca caused by Mg or by a direct effect of the ion on contractile proteins.

Acetylcholine↗

Effects of sulphonylureas on spontaneous motility and induced contractions in rat isolated uterus.

To clarify the action of sulphonylureas on calcium, the effect of tolbutamide and glibenclamide has been investigated on a Ca-dependent process, the contractile activity of uterine smooth muscle. Both sulphonylureas antagonized the contractions evoked by CaCl2 in a non-competitive manner when the uterus was maintained in depolarizing solution and did not affect the spontaneous contractions of rat uterus. The capacity of tolbutamide and glibenclamide to relax vanadate-induced contraction of rat uterus in Ca-free medium suggests that sulphonylureas may have an intracellular site of action related to cytosolic free Ca levels, or effect a reduction in Ca action.

Animals↗

Relaxant effects of sulfonylureas on induced contractions of rat uterine smooth muscle: role of intracellular calcium.

We have investigated the action of tolbutamide and glibenclamide in a Ca-dependent process: the contractile activity of smooth muscle (uterus). The results obtained show that sulfonylureas are capable of relaxing contractions of rat uterus induced by various agents: oxytocin, acetylcholine and KCl in a medium with Ca2+. The capacity of sulfonylureas to also relax oxytocin-induced Ca-free contraction indicates the possibility that the action of these drugs could be due, above all, to a decrease in the intracellular free calcium level. Since maintained contraction induced by oxytocin in a Ca-free solution could be repeated after making a relaxation dose-response curve to sulfonylurea, the most likely mechanism of sulfonylurea-induced uterine relaxation is not an increase in the efflux of Ca but an increase in the Ca-uptake by intracellular organelles.

Acetylcholine↗

Calcium requirement of uterine contraction induced by PGE1: importance of intracellular calcium stores.

The contraction of the rat uterus in response to PGE1 in high K+ medium and in Ca-free solution which contained EDTA has been investigated in order to examine whether excitation-contraction coupling involves the release of Ca from an intracellular store. In uterus maximally contracted by K+, cumulative concentrations of PGE1 (1.25 - 20 ng/ml) caused maintained concentration-dependent contraction. PGE1 induced sustained contraction of rat uterus in Ca-free medium after incubation with 3mM EDTA for 50 min. In these conditions the involvement of extracellular Ca is highly unlikely. The PGE1-induced contraction could be repeated without exposure to external Ca ions and with only slight reduction in magnitude. The PGE1 concentrations required to elicit uterine contraction in Ca-free solution were about 1000 times higher than the effective doses in KCl-depolarized uterus. In conclusion, the present investigation shows that Ca influx is not essential for PGE1-induced contraction of rat uterus, although extracellular Ca enhances it presumably by increasing the free Ca levels in the cytosol.

Alprostadil↗

Effects of chlorpromazine and the antidepressant drugs amitriptyline, clomipramine and mianserin on the Ca-depleted rat uterus.

We have investigated the effect of three antidepressants and one phenothiazine on the EDTA-treated rat uterus. It was found that these drugs induce a sustained contraction of tissue in a Ca-free medium (called Ca-free contraction) at concentrations between 5 X 10(-5) and 1 X 10(-4) M. These responses allowed the construction of dose-response curves. However, higher concentrations caused a relaxation of strips contracted by lower doses previously applied. Oxytocin 1 X 10(-2) IU/ml accelerates the appearance of this relaxation. The antidepressants and chlorpromazine at high doses inhibit the oxytocin-induced Ca-free contraction. The drugs-induced Ca-free contraction could be repeated in the same preparation with only a slight reduction in magnitude.

Amitriptyline↗

[Inhibitory effect of PGE1 on the liberation of insulin induced by glibenclamide].

Glycemia and insulinemia in rat blood samples have been determined at different times before and after administration of glibenclamide, PGE1, glibenclamide and PGE1, glibenclamide and glucose, PGE1 and glucose, and glibenclamide, PGE1 and glucose. PGE1 led to a partial inhibition of glibenclamide induced insulin release, with and without glucose administration, but a total inhibition did not occur. The inhibitory action of PGE1 on insulin secretion was also reflected on the glycemia curves. Defects in insulin release in diabetes could be due in part to an excessive production of PGs, that involve a failure in the beta-cells to respond to glucose signals. The present paper shows that glibenclamide secretory action was not cancelled out by PGE1. These results could explain the availability of glibenclamide in the treatment of diabetes mellitus.

Alprostadil↗