Abstract
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.
Highlights
The optical imaging demonstrated that a medullary longitudinal rostrocaudal column, coincide the rostroventrolateral reticular medulla (RVLM) and the caudal end of ventrolateral medulla, acts as a sympathetic center [1], involved in the generating of resting sympathoexcitatory tone related to arterial pressure control, as well as a vital site of sympathoinhibitory actions of centrally acting antihypertensive agents [2,3]
Obtained data will compare with that obtained from applying similar protocol on halothane anesthetized rats or un-anesthetized sham caudal pressor area (CPA)-stimulated rats, in order to determine whether urethane exert its hypotensive effects centrally and/or peripherally, as well as to interpret the mechanisms by which urethane may exert its hypotensive effect to avoid involvement of urethane with the effects of rostral ventrolateral medulla (RVLM) stimulation
In another experimental protocol designed to investigate the possible role for peripheral α2-adrenoceptors in mediating the hypotensive effect of urethane, the central manipulation of peripheral clonidine hemodynamic effects, was studied in rats divided into three groups each of 6; a) two control groups; a conscious normotensive group of rats to record the basal blood pressure (BP) and HR, and urethane anesthetized group of rats received a vehicles i.v. and intra -RVLM, b) a group of rats anesthetized with urethane (i.p), and administered with clonidine (i.v.) followed by bilaterally injection into the RVLM of either clonidine antagonists, idazoxane or idazoxane+yohimbine
Summary
RVLM ٍْطقت/ الادسٌٍْشجٍنٍت-2- دٗس ّ٘ع اىَخذس فً تاثٍشاث اىنيّ٘ذٌِ اىَؼتَذة ػيى ٍستقبلاث أىفا ُػيى ضغظ اىذً ٗدقاث اىقيب فً اىجشرا. ُ لاٌذاصٗمسا،ُاىٖاى٘ثا، ٍِ اىٍَٕ٘ب،CPA, RVLM،ٌِ اىنيّ٘ذ،ُ ٌ٘سٌثا:اىنيَاث اىذاىت
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