Interaction of clonidine and clonidine analogs with human platelet alpha 2-adrenergic receptors

Steer, M.L.; Atlas, D.

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


ISSN/ISBN: 0006-3002
PMID: 6120721
DOI: 10.1016/0304-4165(82)90145-3
Accession: 043430785

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Several new clonidine analogs were synthesized and their ability to inhibit [3H]phentolamine binding to human platelet alpha 2-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 microM) greater than p-aminoclonidine (0.100 +/- 0.010 microM) greater than hydroxy-phenacetyl-aminoclonidine (0.20 +/- 0.03 microM) greater than p-dansyl clonidine (1.00 +/- 0.20 microM) greater than t-boc-tyrosine clonidine (1.80 +/- 0.60 microM). Thus, p-amino substitution reduces alpha 2-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 alpha 2-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 alpha 2-adrenergic receptors.