[Participation of central and peripheral I1-imidazollinovykh and alpha2-adrenergic receptors in realizing the effects of moxonidine].

The role of the central and peripheral I1-imidazoline and alpha 2-adrenergic receptors in the development of hypotension and bradycardia induced by the intravenous injections of moxonidine was studied, in stroke-prone spontaneously hypertensive (SHR-SP) rats. The intravenous and local injections of I1--alpha 2 antagonist efaroxan (Efa) into the rostral ventrolateral medula (RVLM) abolished the moxonidine-induced fall of blood pressure, but did not eliminate bradycardia. The alpha 2 antagonist yohimbine (Yoh) injected into RVLM did not influence the moxonidine effects, whereas the intravenous Yoh injections fully blocked these effects. Thus the hypotensive action of moxonidine is mediated predominantly by the I1-imidazoline RVMM receptors, while the heart rate decrease is partly realized via the alpha 2 adrenoreceptors of peripheral innervation.