Molderings, G. J. published the artcileInhibitory presynaptic imidazoline receptors on sympathetic nerves in the rabbit aorta differ from I1– and I2-imidazoline binding sites, Quality Control of 2508-72-7, the publication is Naunyn-Schmiedeberg’s Archives of Pharmacology (1995), 351(5), 507-16, database is CAplus and MEDLINE.
The involvement of imidazoline receptors in modulation of noradrenaline release was investigated in the rabbit aorta preincubated with [3H]noradrenaline and superfused with physiol. salt solution containing cocaine, corticosterone and propranolol. After blockade of α2-autoreceptors by rauwolscine, the elec. evoked tritium overflow was inhibited by various imidazolines and guanidines. The rank order of potency was BDF 7579 (4-chloro-2-isoindolinylguanidine) ≥ BDF 6143 (4-chloro-2-(2-imidazolin-2-ylamino)-isoindoline) > BDF 6100 [2-(2-imidazolin-2-ylamino)-isoindoline] > clonidine > ST587 (2-(2-chloro-5-trifluoromethylphenylimino)imidazolidine nitrate) ≥ cirazoline > tolazoline > idazoxan > phentolamine. Comparison of the potencies of these drugs with those previously found for the presynaptic imidazoline receptors in the rabbit pulmonary artery revealed a very good correlation. In contrast, no pos. correlation was found with their affinities for the I1– and I2-imidazoline binding sites in bovine adrenal medullary membranes and with their lipophilicity (log P values). The elec. evoked tritium overflow was also inhibited by the recently identified endogenous imidazoline receptor ligand agmatine, but was not affected by amiloride. In further series of experiments, the ability of putative antagonist at presynaptic imidazoline receptors to counteract the inhibitory effect of imidazoline derivatives was determined Amiloride, imidazole-4-acetic acid and 1-benzylimidazole did not attenuate the inhibitory effect of BDF 6143 on the elec. evoked tritium overflow. In contrast, rauwolscine antagonized the inhibitory effect of various imidazolines; rauwolscine was clearly less potent in antagonizing the effect of clonidine, BDF 6143 and cirazoline (apparent pA2 6.48-7.32) than in antagonizing that of oxymetazoline and moxonidine (apparent pA2 8.33 and 8.12, resp.). In a final series of experiments, BDF 6143 (under the conditions applied a selective agonist at presynaptic imidazoline receptors) proved to be considerably less potent in inhibiting tritium overflow evoked by high K+ than by elec. stimulation, whereas moxonidine (in rabbit aorta a selective agonist at presynaptic α2-adrenoceptors) exhibited similar potency in inhibiting the overflow evoked by both methods of stimulation. It is concluded that noradrenaline release in the rabbit aorta is inhibited via both α2-autoreceptors and presynaptic imidazoline receptors which can be activated by the endogenous imidazoline receptor ligand agmatine. The occurrence of such an α2-adrenoceptor-independent mechanism is compatible with the ability of K+ ions to attenuate the inhibitory effect of an imidazoline receptor agonist but not of an α2-adrenoceptor agonist, since susceptibility to K+ ions has been suggested to be a typical feature of imidazoline recognition sites. The presynaptic imidazoline receptor in rabbit aorta appears to be identical with the previously characterized presynaptic imidazoline receptor in rabbit pulmonary artery, but differs clearly from the I1 and I2 binding sites in the bovine adrenal medulla.
Naunyn-Schmiedeberg’s Archives of Pharmacology published new progress about 2508-72-7. 2508-72-7 belongs to imidazoles-derivatives, auxiliary class Inhibitor,Immunology/Inflammation,Histamine Receptor, name is N-Benzyl-N-((4,5-dihydro-1H-imidazol-2-yl)methyl)aniline hydrochloride, and the molecular formula is C17H20ClN3, Quality Control of 2508-72-7.
Referemce:
https://en.wikipedia.org/wiki/Imidazole,
Imidazole | C3H4N2 – PubChem