Functional properties of agmatine in rat vas deferens

Jurkiewicz, Neide Hyppolito; Carmo, Lúcia Garcez do; Hirata, Hanako; Santos, Wilson C.; Jurkiewicz, Aron

doi:10.1016/0014-2999(96)00274-9

Cited by 24 publications

(11 citation statements)

References 19 publications

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“…The high dose of agmatine also caused complex cardiovascular disturbances, and atipemazole, a specific ␣ 2 -adrenoceptor antagonist, did not influence these effects (Bradley and Headley 1997). In contrast to the results of these studies, agmatine has been shown to have agonist activity at prejunctional ␣ 2 -adrenoceptors in the rat tail artery (Gonzalez et al 1996) and multiple effects on sympathetic neurotransmission in rat vas deferens (Jurkewicz et al 1996). Using different animal species, doses, administration routes, and in vivo or in vitro techniques may be responsible for the discrepancies between the studies.…”

Section: Discussionmentioning

confidence: 65%

Agmatine Potentiates the Analgesic Effect of Morphine by an α2-Adrenoceptor-Mediated Mechanism in Mice

Yeşilyurt

Uzbay

2001

Neuropsychopharmacology

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The effects of agmatine, which is an endogenous polyamine metabolite formed by decarboxylation of L-arginine, and a combination of agmatine and morphine on tail-flick test have been investigated in mice. Adult maleSwiss-Webster mice were used in the study. Agmatine (10, 20 and 40 mg/kg) Agmatine is a cationic amine formed by decarboxylation of arginine by the enzyme arginine decarboxylase (Tabor and Tabor 1984). It is a biological active substance (Lortie et al. 1996) and binds with high affinity to both imidazoline and ␣ 2 -adrenergic receptors of all subclasses (Li et al. 1994;Piletz et al. 1995;Regunathan and Reis 1996;Reis and Regunathan 1998a). Recently, it has been suggested that agmatine meets many criteria for a neurotransmitter in brain. It is synthesised, stored, and released in brain; is contained in neurones and axon terminals; interacts with cell-specific receptors; and elicits biological actions within the central nervous system (Reis and Regunathan 1998a,b). Thus, results of some recent studies indicate the modulatory effects of agmatine in central nervous system. For example, agmatine selectively inhibits nitric oxide synthase (Galea et al. 1996), an enzyme converting L-arginine to nitric oxide, and the NMDA subclass of glutamate receptor channels (Yang and Reis 1999) in rat brain. Several reports indicated that an important role of NMDA receptors and nitric oxide in development of the opioid (Trujillo and Akil 1991;Adams et al. 1993;Thorat et al. 1994;Vaupel et al. 1997) et al. 2000). The drugs that have selective agonistic activity on imidazoline/ ␣ 2 -adrenergic receptors such as clonidine, xylazine, and moxonidine produce antinociceptive responses in rodents (Paalzow 1974;Browning et al. 1982;Ossipov et al. 1989;Fairbanks et al. 2000). The role of adrenoceptors, particularly the ␣ 2 subtype, in the potentiation of opioid-induced analgesia is also well known (Wigdor and Wilcox 1987;Dambisya et al. 1991). In the light of these reports, it would be expected that agmatine, another agent binding imidazoline/ ␣ 2 -receptors, should also have antinociceptive activity. Thus, some recent studies indicate modulatory effects of agmatine on opioid analgesia in mice (Kolesnikov et al. 1996;Fairbanks and Wilcox 1997) and rats (Horváth et al. 1999). It was reported that intrathecal administration of agmatine potentiated morphine-induced ␦ -opioid receptor-mediated analgesia ninefold without affecting pain thresholds and chronic administration prevented 1 -opioid receptor-mediated tolerance in mice (Kolesnikov et al. 1996;Bradley and Headley 1997). However, the mechanisms of these effects remain to be fully understood. It is not certain whether these effects are mediated by ␣ 2 -adrenergic or imidazoline receptors. On the other hand, there are limited studies investigating the antinociceptive effect of peripheral agmatine administration in rodents.The main objective of the present study was to investigate the possible effects of agmatine and an agmatinemorphine combination on nociception by using the tai...

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Section: Discussionmentioning

confidence: 65%

Agmatine Potentiates the Analgesic Effect of Morphine by an α2-Adrenoceptor-Mediated Mechanism in Mice

Yeşilyurt

Uzbay

2001

Neuropsychopharmacology

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“…The activation of α2-adrenoceptors by agonists, like clonidine, inhibits dependence and withdrawal. While agmatine was discovered by its ability to bind to α2-adrenoceptors (Li et al, 1994), several subsequent functional studies reported that agmatine is not an agonist at this site (Pinthong et al, 1995a,b;Jurkiewicz et al, 1996). Moreover, administration of α2-adrenergic agonists, like clonidine, while blocking opiate withdrawal, also causes sympathetic inhibition and reduction in arterial pressure (Gatti et al, 1988;Hieble and Kolpak, 1993).…”

Section: Discussionmentioning

confidence: 99%

Effect of agmatine on the development of morphine dependence in rats: potential role of cAMP system

Arıcıoğlu

Means

Regunathan

2004

European Journal of Pharmacology

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Agmatine is an endogenous amine derived from arginine that potentiates morphine analgesia and blocks symptoms of naloxone-precipitated morphine withdrawal in rats. In this study, we sought to determine whether treatment with agmatine during the development of morphine dependence inhibits the withdrawal symptoms and that the effect is mediated by cAMP system. Exposure of rats to morphine for 7 days resulted in marked naloxone-induced withdrawal symptoms and agmatine treatment along with morphine significantly decreasing the withdrawal symptoms. The levels of cAMP were markedly increased in morphine-treated rat brain slices when incubated with naloxone and this increase was significantly reduced in rats treated with morphine and agmatine. The induction of tyrosine hydroxylase after morphine exposure was also reduced in locus coeruleus when agmatine was administered along with morphine. We conclude that agmatine reduces the development of dependence to morphine and that this effect is probably mediated by the inhibition of cAMP signaling pathway during chronic morphine exposure.

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“…It has been suggested that agmatine acts as an endogenous agonist at imidazoline receptors and as a noncatecholamine ligand at a 2 -adrenergic receptors (Li et al, 1994;Piletz et al, 1995). Agmatine and a 2 -adrenoceptors have important functional interactions, including the potentiating effect on morphineinduced analgesia (Fairbanks et al, 2000;Yesilyurt and Uzbay, 2001), agonistic activity in prejunctional rat tail artery (Gonzalez et al, 1996), and multiple effects on sympathetic neurotransmission in rat vas deferens (Jurkiewicz et al, 1996). Involvement of a 2 -adrenoceptors in anticonvulsant properties of agmatine has been recently shown (Demehri et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Agmatine Potentiates Morphine-Induced Conditioned Place Preference in Mice: Modulation by Alpha(2)-Adrenoceptors

Tahsili-Fahadan

Yahyavi-Firouz-Abadi

Khoshnoodi

et al. 2005

Neuropsychopharmacol

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The effects of agmatine, an endogenous polyamine metabolite formed by decarboxylation of L-arginine, and its combination with morphine on conditioned place preference (CPP) has been investigated in male mice. Our data show that subcutaneous administration of morphine (1-7.5 mg/kg) significantly increases the time spent in the drug-paired compartment in a dose-dependent manner. Intraperitoneal administration of agmatine (1-40 mg/kg) alone does not induce either CPP or conditioned place aversion, while combination of agmatine and subeffective doses of morphine leads to potent rewarding effects. Lower doses of morphine (0.1, 0.05, and 0.01 mg/kg) are able to induce CPP in mice pretreated with agmatine 1, 5, and 10 mg/kg, respectively. Concomitant intraperitoneal administration of UK 14 304 (0.5 mg/kg), a highly selective a 2 -agonist, with per se noneffective dose of morphine (0.5 mg/kg) and also its combination with noneffective doses of agmatine (1 mg/kg) plus morphine (0.05 mg/kg) produces significant CPP. UK 14 304 (0.05, 0.5 mg/kg) alone, or in combination with agmatine (1, 5 mg/kg) have had no effect. We have further investigated the possible involvement of the a 2 -adrenoceptors in the potentiating effect of agmatine on morphine-induced place preference. Selective a 2 -antagonists, yohimbine (0.005 mg/kg) and RX821002 (0.1, 0.5 mg/kg), block the CPP induced by concomitant administration of agmatine (5 mg/kg) and morphine (0.05 mg/kg). Yohimbine (0.001-0.05 mg/kg) or RX821002 (0.05-0.5 mg/kg) alone or in combination with morphine (0.05 mg/kg) or agmatine (5 mg/kg) fail to show any significant place preference or aversion. Our results indicate that pretreatment of animals with agmatine enhances the rewarding properties of morphine via a mechanism which may involve a 2 -adrenergic receptors.

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Functional properties of agmatine in rat vas deferens

Cited by 24 publications

References 19 publications

Agmatine Potentiates the Analgesic Effect of Morphine by an α2-Adrenoceptor-Mediated Mechanism in Mice

Agmatine Potentiates the Analgesic Effect of Morphine by an α2-Adrenoceptor-Mediated Mechanism in Mice

Effect of agmatine on the development of morphine dependence in rats: potential role of cAMP system

Agmatine Potentiates Morphine-Induced Conditioned Place Preference in Mice: Modulation by Alpha(2)-Adrenoceptors

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