Interaction of clonidine and clonidine analogs with human platelet α2-adrenergic receptors

Steer, M; Atlas, D

Biochimica et Biophysica Acta - General Subjects 714(3): 389-394


ISSN/ISBN: 0304-4165
DOI: 10.1016/0304-4165(82)90145-3
Accession: 061674843

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Several new clonidine analogs were synthesized and their ability to inhibit [3H] phentolamine binding to human platelet α2-adrenergic receptors was tested. The order of potency and calculated dissociation constants for clonidine and its analogs were as follows: clonidine (0.020 ± 0.005 μM) >p-aminoclonidine (0.100 ± 0.010 μM) > hydroxy-phenacetyl-aminoclonidine (0.20 ± 0.03 μM) >p-dansyl clonidine (1.00 ± 0.20 μM) >t-boc-tyrosine clonidine (1.80 ± 0.60 μM). Thus, p-amino substitution reduces α2-adrenergic affinity in the platelet system. The effects of clonidine and its p-amino analogs on platelet adenylate cyclase were also evaluated. This enzyme is inhibited by epinephrine acting via α2-adrenergic receptors. Both clonidine and p-aminoclonidine cause slight inhibition of basal adenylate cyclase and reverse the inhibition induced by epinephrine. These observations indicate that clonidine is a partial agonist for platelet α2-adrenergic receptors.