Navegando por Palavras-chave "agmatine"

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    Blockade by agmatine of catecholamine release from chromaffin cells is unrelated to imidazoline receptors
    (Elsevier B.V., 2001-04-06) Santos, W. C.; Hernandez-Guijo, J. M.; Ruiz-Nuno, A.; Olivares, R.; Jurkiewicz, A.; Gandia, L.; Garcia, A. G.; Univ Autonoma Madrid; Universidade Federal de São Paulo (UNIFESP); Univ Amazonas; Hosp Princesa
    The blockade of exocytosis induced by the putative endogenous ligand for imidazoline receptors, agmatine, was studied by using on-line measurement of catecholamine release in bovine adrenal medullary chromaffin cells. Agmatine inhibited the acetylcholine-evoked release of catecholamines in a concentration-dependent manner (IC50 = 366 muM); the K+-evoked release of catecholamines was unaffected. Clonidine (100 muM) and moxonidine (100 muM) also inhibited by 75% and 50%, respectively, the acetylcholine-evoked response. in cells voltage-clamped at -80 mV, the intermittent application of acetylcholine pulses elicited whole-cell inward currents (I-ACh) that were blocked 63% by 1 mM agmatine. the onset of blockade was very fast (tau (on) = 31 ms); the recovery of the current after washout of agmatine also occurred very rapidly (tau (off) = 39 ms). Efaroxan (10 muM) did not affect the inhibition of I-ACh elicited by 1 mM agmatine. I-ACh was blocked 90% by 100 muM clonidine and 50% by 100 muM moxonidine. the concentration-response curve for acetylcholine to elicit inward currents was shifted to the right in a non-parallel manner by 300 muM agmatine. the blockade of I-ACh caused by agmatine (100 muM) was similar at various holding potentials, around 50%. When intracellularly applied, agmatine did not block I-ACh. At 1 mM, agmatine blocked I-Na by 23%, I-Ba by 14%, I-K(Ca) by 16%, and I-K(VD) by 18%. in conclusion, agmatine blocks exocytosis in chromaffin cells by blocking nicotinic acetylcholine receptor currents. in contrast to previous views, these effects seem to be unrelated to imidazoline receptors. (C) 2001 Elsevier Science B.V. All rights reserved.
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    Functional properties of agmatine in rat vas deferens
    (Elsevier B.V., 1996-07-04) Jurkiewicz, N. H.; doCarmo, L. G.; Hirata, H.; Santos, W. D.; Jurkiewicz, A.; Universidade Federal de São Paulo (UNIFESP)
    Experiments were performed with rat vas deferens to verify whether agmatine, an endogenous ligand for adrenoceptors and imidazoline receptors, can influence sympathetic neurotransmission, with respect to contractions induced by transmural nerve stimulation, contractions induced by exogenous noradrenaline, and overflow of endogenous noradrenaline. It was shown that agmatine (a) caused a dose-dependent potentiation of electrically induced twitches, up to about 70% in relation to controls, (b) shifted to the right the inhibitory concentration-response curves for clonidine on electrically induced twitches, indicating competitive antagonism at presynaptic ol-adrenoceptors, with a pA(2) value of 4.12 +/- 0.10, (c) shifted to the right the concentration-response curves for noradrenaline-induced contractions, indicating competitive antagonism at postsynaptic alpha-adrenoceptors as well, with a pA(2) value of 4.03 +/- 0.10, and (d) caused a dose-dependent increase of KCl-induced overflow of noradrenaline, up to about 90% in relation to controls. It is concluded that agmatine has multiple effects on sympathetic neurotransmission in rat vas deferens.
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    L-NAME pre-treatment partially inhibits the agmatine-evoked depression of the electrically induced twitch contraction of isolated rat vas deferens
    (Elsevier B.V., 2006-07-24) Garcez-do-Carmo, Lucia; Santos, Wilson C.; Universidade Federal Fluminense (UFF); Universidade Federal de São Paulo (UNIFESP)
    The effect of the putative endogenous ligand for alpha(2)-adrenoceptors and imidazoline receptors agmatine was studied in sympathetic neurotransmission in the rat epididymal vas deferens. Tissues were obtained from N-omega-nitro-L-arginine methyl ester (L-NAME)-treated or normal animals and were contracted by electrical stimulation or by exogenous adenosine 5'-triphosphate (ATP). in the electrically stimulated epididymal end, agmatine produced an inhibitory effect on twitch contraction that was partially reversed in L-NAME-treated animals, whereas the inhibition produced by clonidine was not affected by L-NAME treatment. the nitric oxide (NO)-donor S-nitroso-N-acetyl-penicillamine (SNAP) also inhibited twitch contraction. Neither agmatine nor SNAP interfered with the responses induced by exogenous ATP in the epididymal end. Removal of the epithelium of the preparation did not modify the agmatine response. We conclude that a nitrergic pathway activated by agmatine plays a role in its inhibitory effect in rat vas deferens, but it remains to be investigated whether it results from a direct action on the enzyme NO-synthase or a receptor-mediated mechanism. (c) 2006 Elsevier Inc. All rights reserved.
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    Use of transgenic (knockout) mice reveals a site distinct from the alpha(2A)-adrenoceptors for agmatine in the vas deferens
    (Polish Acad Sciences Inst Pharmacology, 2009-03-01) Santos, Wilson da Costa; Garcez-do-Carmo, Lucia [UNIFESP]; Silva, Eliane Cristina da [UNIFESP]; Pascual, Ricardo de; Jurkiewicz, Neide Hyppolito [UNIFESP]; Jurkiewicz, Aron [UNIFESP]; Gandia, Luis; Universidade Federal Fluminense (UFF); Universidade Federal de São Paulo (UNIFESP); Fac Med
    The inhibitory effect of agmatine on electrically induced contractions was studied in vas deferens of Adra 2a transgenic mice lacking alpha(2A)-adrenoceptors. Agmatine and clonidine caused a concentration-dependent inhibition of twitches. However, while agmatine showed a similar pIC(50) value in control and transgenic mice, the pIC(50) value for clonidine was about 30-fold lower in knockout mice. In both strains, yohimbine shifted the curve for clonidine, but not for agmatine, even when a 100-fold higher concentration of yohimbine was employed. Our results indicate that inhibition by agmatine in mouse vas deferens is not simply due to interactions with alpha(2)-adrenoceptors in our experimental conditions.