Examinando por Autor "Arribas, Silvia"

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Effect of phorbol esters on noradrenaline release from cerebral arteries
(Elsevier, 1989-01-16) Balfagón, Gloria; de Sagarra, M Rosa; Barrús, M Teresa; Arribas, Silvia; Capilla, M Isabel; Marín, Jesús
Abstract The effect of phorbol 12-myristate, 13-acetate (PMA), an activator of protein kinase C, on noradrenaline (NA) release from cat cerebral arteries preincubated with [3H]NA was investigated in order to examine the role of that enzyme in this secretion. PMA (3 μM) potentiated tritium release elicited by electrical stimulation (2 Hz, 0.3 ms) without modification of spontaneous secretion, whereas 4α-phorbol 12,13 didecanoate (3 μM), an inactive compound, had no effect. Tritium release evoked by tyramine was not modified by PMA. The electrically evoked tritium secretion was reduced by clonidine (1 μM) or B-HT 920 (0.1 μM), α2-adrenoceptor agonists, and unaffected by yohimbine (1 μM), an α2-adrenoceptor antagonist. The presence of clonidine, B-HT 920 or yohimbine reduced the action of PMA. The facilitatory effect of PMA was not increased by the Ca2+ ionophore A23187 (5 μM). These results suggest that: (1) protein kinase C of perivascular adrenergic nerve endings participates in the exocytotic release of NA; (2) the effects of PMA could be partially due to an interference with prejunctional autoinhibitory α2-adrenoceptors, and (3) the increase of intracellular Ca2+ produced by A23187 appears to be inadequate for potentiating the action of PMA.
Endothelial Modulation of Ouabain-lnduced Contraction and Sodium Pump Activity in Aortas of Normotensive Wystar-Kyoto and Spontaneously Hypertensive Rats
(Karger Publishers, 1996) Ponte, Ana; Marín, Jesús; Arribas, Silvia; González-Carnicero, Rita; Barrús, M Teresa; Salaices, Mercedes; Sánchez-Ferrer, Carlos F
The influence of vascular endothelium on ouabain-induced contractions and sodium pump activity in aortic segments of Wistar-Kyoto (WKY) and spontaneously hypertensive rat (SHR) was analyzed. De-endothelialization increased and reduced ouabain-induced contractions in WKY and SHR segments, respectively. The effects of de-endothelialization were not reproduced by pretreatment of the segments with NG-nitro-L-arginine methyl ester, indo-methacin, or 5, 8, 11, 14-eicosatetraenoic acid, acetyl salicylic acid, dazoxiben, phosphoramidon, BQ-123, or superoxide dismutase. Bioassay experiments suggest that ouabain releases a diffusible factor from endothelial cells that inhibits or facilitates digitalis-induced contractions in WKY and SHR segments, respectively. In a potassium-free solution, potassium-induced relaxation in segments of both strains was abolished by ouabain in de-endothelialized aortas and reduced in intact ones. Ouabain-sensitive 86Rb+ uptake was significantly reduced by de-endothelialization both in WKY and in SHR. These results suggest that the vascular endothelium of WKY and SHR aortas releases a diffusible factor that stimulates the sodium pump and/or protects it from ouabain blockade. Ouabain also releases a diffusible endothelium-derived factor in SHR aortas that facilitates ouabain-induced contractions.