Imidazoline receptors associated with noradrenergic terminals in the rostral ventrolateral medulla mediate the hypotensive responses of moxonidine but not clonidine.

摘要: We determined whether the cardiovascular actions of central anti-hypertensive agents clonidine and moxonidine are dependent on noradrenergic or serotonergic innervation rostral ventrolateral medulla (RVLM) in conscious rabbits. 6-Hydroxydopamine (6-OHDA) 5,6-dihydroxytriptamine (5,6-DHT) was injected into RVLM to deplete terminals respectively. One, 2 4 weeks later, responses fourth ventricular (4V) (0.65 microg/kg) (0.44 were examined. Destruction pathways by 6-OHDA reduced hypotensive response 4V 62%, 47% 60% that observed vehicle treated rabbits at 1, The induced bradycardia similarly attenuated (to 46% vehicle). Conversely, had no effect bradycardic effects clonidine. Efaroxan (I(1)-imidazoline receptor/alpha(2)-adrenoceptor antagonist; 3.5, 11, 35 2-methoxyidazoxan (alpha(2)-adrenoceptor 0.3, 0.9, 3 equally reversed hypotension clonidine, suggesting a mainly alpha(2)-adrenoceptor mechanism. preferentially both 5,6-DHT groups 1st week after 6-OHDA, mechanism involving I(1)-imidazoline receptors. This selectivity subsequently lost 2nd 4th when remaining mediated alpha(2)-adrenoceptors. Depletion did not alter either agonist nor it change relative effectiveness antagonists. Western blots tissues probed with imidazoline antisera showed pattern bands close reported other species. main an 18% lower level 42 kDa protein (P<0.05). conclude but through receptors intact within RVLM. Furthermore, may be associated receptor protein.