Anyone using agamatine over L-Arginine??

[Armanilexi]

I've been hearing some good things and reading even better things about agamatine and thinking about using that instead of arginine. I was curious to know if anyone else has tried it or currently using it and what results have they had

[corageon]

Agmatine is over-rated IMO - it also can actually reduce nitric oxide..it basically acts like Clonidine which is an anti-hypertensive/anti-anxiety drug.

Neuropharmacology. 2003 Sep;45(4):534-42.Agmatine exerts anticonvulsant effect in mice: modulation by alpha 2-adrenoceptors and nitric oxide.

Demehri S1, Homayoun H, Honar H, Riazi K, Vafaie K, Roushanzamir F, Dehpour AR.
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Abstract

The effect of agmatine, an endogenous polyamine metabolite, on seizure susceptibility was investigated in mice. Acute intraperitoneal administration of agmatine (5, 10, 20, 40 mg/kg) had a significant and dose-dependent inhibitory effect on pentylenetetrazole (PTZ)-induced seizures. The peak of this anticonvulsant effect was 45 min after agmatine administration. We further investigated the possible involvement of the alpha(2)-adrenoceptors and L-arginine/NO pathway in this effect of agmatine. The alpha(2)-adrenoceptor antagonist, yohimbine (0.5-2 mg/kg), induced a dose-dependent blockade of the anticonvulsant effect of agmatine. The nitric oxide synthase (NOS) substrate, L-arginine (60 mg/kg), inhibited the anticonvulsant property of agmatine and this effect was significantly reversed by NOS inhibitor N(G)-nitro-L-arginine (L-NAME, 30 mg/kg), implying an NO-dependent mechanism for L-arginine effect. We further examined a possible additive effect between agmatine (1 or 5 mg/kg) and L-NAME (10 mg/kg). The combination of L-NAME (10 mg/kg) with agmatine (5 but not 1 mg/kg) induced a significantly higher level of seizure protection as compared with each drug alone. Moreover, a combination of lower doses of yohimbine (0.5 mg/kg) and L-arginine (30 mg/kg) also significantly decreased the anticonvulsant effect of agmatine. In conclusion, the present data suggest that agmatine may be of potential use in seizure treatment.


PMID:12907314[PubMed - indexed for MEDLINE]

Neurochem Int. 1997 Jan;30(1):37-45.Central cardiovascular actions of agmatine, a putative clonidine-displacing substance, in conscious rabbits.
Head GA1, Chan CK, Godwin SJ.
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Abstract
Agmatine, an endogenous clonidine-displacing substance, has been shown to have an affinity for both alpha 2-adrenoceptors and imidazoline receptors (IR). In conscious rabbits, we have examined the cardiovascular effects of agmatine and its interaction with clonidine, a presumed agonist and 2-methoxyidazoxan, an antagonist at alpha 2-adrenoceptors. We have also examined the effect of agmatine on agents having high affinity for I1-imidazoline receptors namely moxonidine (agonist) and efaroxan (antagonist). Initial dose-response studies showed that agmatine administered in low doses (0.01-10 micrograms/kg) into the fourth ventricle did not change mean arterial pressure but did produce a dose-dependent bradycardia (maximum -16 +/- 3 beats/min). A higher dose of 100 micrograms/kg produced an adverse reaction in the conscious animals accompanied by a marked increase in mean arterial pressure and a reversal of the bradycardia. This is in contrast to the effects of fourth ventricular clonidine and moxonidine, which caused a dose-dependent fall in both mean arterial pressure and heart rate. Agmatine when administered at the highest well-tolerated dose of 10 micrograms/kg did not further alter the clonidine-induced hypotension but produced a greater bradycardia (-12 +/- 4 beats/min clonidine; -29 +/- 4 beats/min clonidine plus agmatine; p < 0.05). Similarly, the hypotension induced by moxonidine was not altered by agmatine but heart rate was reduced after the addition of agmatine (p < 0.01). Efaroxan and 2-methoxy-idazoxan, at doses which produced no effects when given alone, similarly reversed the fall in heart rate elicited by agmatine and caused a small but significant rise in mean arterial pressure. We have previously shown that the doses of these antagonists used in this study produce an equal reversal of the bradycardia induced by fourth ventricular alpha-methyldopa (alpha 2-adrenoceptor agonist) and clonidine and hence have similar alpha 2-adrenoceptor blocking effects. Our results show that agmatine produces bradycardia as does moxonidine and clonidine but does not mimic or block the hypotensive responses to these agents. These findings do not support the hypothesis that agmatine is an endogenous ligand for IR. However, the bradycardia induced by agmatine may be mediated via alpha 2-adrenoceptors since it was equally blocked by efaroxan and 2-methoxy-idazoxan. Thus while alpha 2-adrenoceptor actions of agmatine on heart rate are evident at relatively low doses, the reason for the lack of alpha 2-adrenoceptor mediated hypotension is not known.
PMID: 9116586 [PubMed - indexed for MEDLINE]