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Imidazole receptors and clonidine-displacing substance in relationship to control of blood pressure, neuroprotection, and adrenomedullary secretion.

Clonidine, idazoxan, rilmenidine, and comparable agents bind to imidazol(in)e (IR), as well as alpha 2-adrenergic, receptors. Interaction with IRs mediates the hypotension elicited by these drugs at their site of action in the rostral ventrolateral medulla oblongata (RVL) and probably the neuroprotection in focal ischemic cerebral infarction. Unlike alpha 2-adrenergic receptors, IRs are not coupled to G-proteins. Their native ligand may be clonidine-displacing substance (CDS), a potent, partially purified adrenomedullary secretagogue, distributed regionally in brain and some peripheral organs. IRs and CDS may be important in the genesis, expression, and/or therapy of hypertension and stroke.