Contribution of imidazoline receptors and α2-adrenoceptors in the rostral ventrolateral medulla to sympathetic baroreflex inhibition by systemic rilmenidine


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Abstract

ObjectivesTo determine whether the hypotensive and sympathetic baroreflex inhibition by rilmenidine administered systemically are mediated via imidazoline receptors in the rostral ventrolateral medulla (RVLM).MethodsInitial dose–response curves to rilmenidine were determined in urethane anaesthetized rabbits. Effects of a single intravenous dose of rilmenidine (445 μg/kg) on the renal sympathetic nerve activity (RSNA) baroreflex were examined before and after microinjection into the RVLM of the mixed imidazoline/α2-adrenoceptor antagonist idazoxan and the α2-adrenoceptor antagonist 2-methoxyidazoxan (2-MI).ResultsIntravenous administration of rilmenidine lowered mean arterial pressure and RSNA, inhibited the RSNA baroreflex range by 33% and shifted the baroreflex curve to the left. Idazoxan injected into the RVLM reversed the hypotension and completely restored the baroreflex curve at doses that did not affect the hypotension produced by the selective α2-adrenoceptor agonist α-methylnoradrenaline. The α2-adrenoceptor antagonist, 2-MI also reversed the rilmenidine sympatho-inhibition suggesting that α2-adrenoceptors are activated as well.ConclusionsThe results of the present study show that the hypotensive and sympatho-inhibitory actions of systemic rilmenidine are primarily mediated via imidazoline receptors in the RVLM. However, α2-adrenoceptors are also involved, probably as a direct result of the imidazoline receptor action.

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