Browsing by Author "Tapia, W"

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    Does the release of tritiated noradrenaline accurately reflect the release of endogenous noradrenaline from rat vas deferens nerve terminals?
    (1997) Bitran, M; Tapia, W
    To determine whether the release of tritiated noradrenaline (NA) front the sympathetic nerve terminals of the rat vas deferens is art accurate reflection of the release of endogenous NA, we compared the electrically-evoked release of tritiated and endogenous NA front the prostatic sections of the vasa deferentia of male rats.
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    Neuropeptide Y induced inhibition of noradrenaline release in rat hypothalamus
    (1999) Bitran, M; Tapia, W; Eugenín, E; Orio, P; Boric, MP
    We aimed at characterizing the receptor subtype and the signaling pathway involved in the inhibitory effect of neuropeptide Y on the release of endogenous noradrenaline from rat hypothalamus. Slices of hypothalamus were stimulated with two trains of electrical pulses, and the release of noradrenaline and nitric oxide was measured, The electrical stimulation of hypothalamic slices induced a consistent release of both endogenous noradrenaline and NO. Neuropeptide Y inhibited concentration dependently the stimulated noradrenaline release. Similarly, agonists for neuropeptide Y Y-2, Y-2 and Y-5 receptors inhibited noradrenaline release, albeit with a potency lower than neuropeptide Y. GW1229, a selective neuropeptide Y Y-1 receptor antagonist counteracted the effect of neuropeptide Y, but not that of PYY-(3-36), an agonist active at neuropeptide Y Y-5 and Y-2 receptors. These results indicate that the inhibitory effect of neuropeptide Y is likely mediated by several receptor subtypes, including neuropeptide Y Y-2, Y-5 and possibly Y-2 receptors. One mu M NPY significantly enhanced NO release induced by the electrical stimulation. N-G-monomethyl-L-arginine, an inhibitor of nitric oxide synthase, abolished NO release and blocked the inhibitory effect of neuropeptide Y on noradrenaline release. We conclude that nitric oxide participates in the signaling pathway of neuropeptide Y in the rat hypothalamus. (C) 1999 Elsevier Science B.V. All rights reserved.
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    Neuropeptide Y inhibits (3)[H]noradrenaline release in the rat vas deferens independently of cAMP levels
    (1996) Bitran, M; Torres, G; Tapia, W; HuidobroToro, JP
    The purpose of the present investigation was to ascertain the functional significance of the reduction in cyclic AMP (cAMP) levels in the inhibitory action of neuropeptide Y (NPY) on [H-3]noradrenaline ([H-3]NA) release, as well as to further characterize the subtype(s) of NPY receptors involved in the peptide's actions in the rat vas deferens. We studied the effects of NPY, carboxyterminal fragments of this peptide and the NPY analog [Leu(31),Pro(34)]-NPY on three functional responses, namely, the release of [H-3]NA and the associated muscle contractions evoked by electrical stimulation, and the accumulation of cAMP stimulated by forskolin. NPY, a known inhibitor of the electrically-evoked [H-3]NA release and neurogenic contractions is also a potent inhibitor of the forskolin-stimulated cAMP synthesis in the prostatic portion of the rat vas deferens. However, the ability of NPY to inhibit cAMP accumulation is lost upon tissue denervation, suggesting that this is likely to be a prejunctional effect. Elevation of cAMP levels by the use of the cell permeant analog of cAMP, 8-(p-chlorophenylthio)-cAMP (8pCPTcAMP) increases the electrically-evoked release of [H-3]NA. However, the inhibition of [H-3]NA release by NPY is not prevented by 8pCPTcAMP. Structure-activity relationship studies reveal that NPY and related peptides inhibit the release of [H-3]NA, the muscle contractions and the synthesis of cAMP with a similar pharmacological profile. NPY is the most potent inhibitory agent, whereas [Leu(31),Pro(34)]-NPY and NPY13-36, the respective Y-1 and Y-2 selective agonists, display similar potencies to inhibit the three responses. It is concluded that NPY inhibits neurotransmission in the rat vas deferens through the activation of a peptide receptor different from the known NPY-Y-1 or NPY-Y-2 receptor subtypes. NPY receptor activation in the vas deferens is negatively coupled to adenylyl cyclase activity. This intracellular signalling pathway is, however, not likely to mediate the peptide effects on the prejunctional regulation of noradrenaline release.