Comparison of the interaction of agmatine and crude methanolic extracts of bovine lung and brain with α<sub>2</sub>‐adrenoceptor binding sites

Pinthong, Darawan; Hussain, Javaid; Kendall, David A.; Wilson, V.G.

doi:10.1111/j.1476-5381.1995.tb14988.x

Cited by 30 publications

(27 citation statements)

References 24 publications

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“…As agmatine does not bind to opiate receptors, these actions are not mediated by direct effect on opiate receptors (Bradley and Headley, 1997). The abilities of agmatine to bind to α2-adrenoceptors (Li et al, 1994;Pinthong et al, 1995a;Pinthong et al, 1995b;Piletz et al, 1995) and to block NMDA receptor channels (Yang and Reis, 1999) or inhibit nitric oxide synthase (NOS; Galea et al, 1996;Li et al, 1999a;Demady et al, 2001) were considered as potential mechanisms for these actions. We have recently reported that acute administration of agmatine just before withdrawal failed to reverse centrally mediated withdrawal symptoms to morphine in neuronal NOS (nNOS)-deficient transgenic mice while it was preventing peripheral withdrawal symptoms (Aricioglu et al, 2004).…”

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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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 binds to alpha 2-adrenergic receptors of all subclasses and to imidazoline receptors of the I 1 -and I 2 -subclasses. [13][14][15] It is not known whether agmatine is an agonist and/or antagonist at any receptor, but most endogenous ligands are agonists. The simplest explanation for our findings is that agmatine exerts its effect either by acting on presynaptic alpha 2-adrenoceptors or by acting on imidazoline receptors.…”

Section: Discussionmentioning

confidence: 99%

Enhancement of EFS-induced contractions, by agmatine, in guinea pig gallbladder smooth muscle strips

et al. 2005

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“…Conversely, the contractile response induced by serum CDS extracts in aortic tissue preparations was not blocked by the selective α 2 -AR antagonist rauwolscine [36]; illustrating that CDS does not exert its effect via α 2 -AR. Interestingly, whilst some groups reported that CDS elicits opposing effects to clonidine, others demonstrated the lack of clonidine-like properties of CDS [37,38]. The reported differences in CDS-evoked responses may be due to the variation in extraction techniques used to isolate and purify CDS, as well as the use of various tissue sources that has led to the ambiguity of its definitive role.…”

Section: The Endogenous Extract At Imidazoline Binding Sites: Clonidimentioning

confidence: 91%

Borne Identity: Leading Endogenous Suspects at Imidazoline Binding Sites

Ghazaleh¹,

Tyacke²,

Hudson³

2015

J Neurol Neurosci

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The imidazoline binding sites (I-BS) represent a heterogenous family of receptors/sites that stemmed from studies investigating the hypotensive effect of the imidazoline compound clonidine [1]. Structure-affinity relationship studies complemented by functional analyses characterised three types of I-BS, denoted I 1 -BS, I 2 -BS (I 2A and I 2B ) and I 3 -BS [2]. Extensive research has established the involvement of central I 1 -BS in cardiovascular function [3]. Other reported functions include alleviating symptoms associated with metabolic syndrome X [4] and Huntington's Disease [5], promoting natriuresis [6], regulating intraocular pressure [7], and modulating mRNA expression for phenylethanolamine N-methyl transferase (PNMT) [8]. Furthermore, the expression of these sites was shown to be altered in conditions such as depression [9] and dysphoric premenstrual syndrome [10] AbstractOver the past few years, a vast amount of research has shed light on the pharmacology of imidazoline binding sites (I-BS). To date, at least three classes of imidazoline binding sites have been characterised in accordance to their localisation, drug selectivity, proposed signalling pathways and functional roles. The existence of these sites raises the question as to whether an endogenous modulator exists. The identification of an endogenous extract denoted as clonidine displacing substance prompted the search for the active ingredient capable of mimicking the action of selective ligands at these sites. A number of candidates have been isolated and their functional activities have been assessed at these sites. Such endogenous ligands include agmatine, imidazoleacetic acid ribotide and the β-carboline harmane. As of yet, no consensus has been made to confirm the identity of the endogenous ligand at I-BS. The current review collates and reports what is known about these substances and their functional significance at I-BS.

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Comparison of the interaction of agmatine and crude methanolic extracts of bovine lung and brain with α₂‐adrenoceptor binding sites

Cited by 30 publications

References 24 publications

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

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

Enhancement of EFS-induced contractions, by agmatine, in guinea pig gallbladder smooth muscle strips

Borne Identity: Leading Endogenous Suspects at Imidazoline Binding Sites

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Comparison of the interaction of agmatine and crude methanolic extracts of bovine lung and brain with α2‐adrenoceptor binding sites

Cited by 30 publications

References 24 publications

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

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

Enhancement of EFS-induced contractions, by agmatine, in guinea pig gallbladder smooth muscle strips

Borne Identity: Leading Endogenous Suspects at Imidazoline Binding Sites

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Comparison of the interaction of agmatine and crude methanolic extracts of bovine lung and brain with α₂‐adrenoceptor binding sites