Utilize este identificador para referenciar este registo: http://hdl.handle.net/10451/21210
Título: Phenylephrine induces endogenous noradrenaline release in the rat vas deferens through nitric oxide synthase pathway
Autor: Pinto, R
Barrento, C
Mota-Filipe, H
Lima, BS
Palavras-chave: Pharmacology & Pharmacy
Toxicology
Data: 2003
Editora: BLACKWELL MUNKSGAARD
Citação: PHARMACOLOGY & TOXICOLOGY. - Vol. 93, n. 4 (OCT 2003), p. 191-196
Resumo: We have previously observed that in the rat vas deferens nitric oxide synthase pathway potentiated phenylephrine-induced contractility raising the possibility of a facilitatory role on neurotransmission by nitric oxide. To confirm this hypothesis we studied the effect of phenylephrine on the concentration response curves obtained in preparations from reserpine-treated rats in the absence and presence of the nitric oxide synthase inhibitor N-G-monomethyl-L-arginine (L-NMMA). The endogenous noradrenaline released by normal preparations (without reserpine) was measured in the perfusion fluid of preparations stimulated with phenylephrine, in the absence and presence of L-NMMA, L-NMMA + the nitric oxide donor 3-morpholinosydnonimine hydrochloride (SIN-1), the alpha(1)-adrenoceptor antagonist prazosin and the blocker of noradrenaline carrier desipramine. The phenylephrine-induced noradrenaline release in a calcium-free medium was also measured. L-NMMA decreased the E-max of phenylephrine concentration response curves obtained in preparations from normal (reserpine-untreated) but not from reserpine-treated rats. In the perfusion fluid of preparations incubated with phenylephrine, a concentration-dependent increase of noradrenaline was observed which was reversed by L-NMMA and restored when SIN-1 was added together with the nitric oxide synthase inhibitor. The concentration-dependent phenylephrine-induced noradrenaline increase was not modified by desipramine but was abolished by 10 muM prazosin. In calcium-free medium, phenylephrine failed to increase the noradrenaline concentration. These results suggest that in the rat vas deferens, nitric oxide pathway potentiates the phenylephrine-induced contractility through a mechanism which involves calcium-dependent release of endogenous noradrenaline and seems to depend, at least partially on the activation of alpha(1)-adrenoceptors.
URI: http://hdl.handle.net/10451/21210
ISSN: 0901-9928
Aparece nas colecções:FF - Produção Científica 2000-2009

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