Role of the anesthetic determine the clonidine effects mediated by RVLM -α2-adrenoceptors on blood pressure and heart rate in rats

Abstract EN

To examine the hypothesis of a role for α2-adrenoceptors in mediating the mechanism of urethane hypotensive effect whether it's peripheral or central, Wistar rats were anesthetized with urethane or (for comparison) with halothane, to study the influence of urethane that govern the mechanism of central and peripheral α2-adrenoceptors action, on basal BP & HR, and the rise in blood pressure (BP) to the stimulation of caudal pressor area (CPA), when these receptors were either centrally activated by bilateral rostral ventrolateral medulla (RVLM) microinjection of clonidine (30nM), and blockade with any of the clonidine antagonists, yohimbine (500pmol/50nl), and idazoxane (270nM) or yohimbine+idazoxane, or when peripherally activated (of urethane anesthetized rats) by i.v.

clonidine (100nmol/kg), which also blockade with idazoxane or yohimbine+idazoxane.

The results indicated presence of no anesthetic differences in a partial involvement of α2-receptors-RVLM, vs.

a complete involvement of I(1)-imidazole receptors in mediating the hypotensive effects of clonidine.

It also indicates α2-/I(1)-receptors synergism in raising the urethane lowering of baseline of SBP to the levels of control or halothane group.

In conclusion, the result suggests involvement both of the central and the peripheral α2-adrenoceptors in mediating urethane hypotensive effects.