Watkins L, Maixner W
Department of Pharmacology, University of North Carolina, Chapel Hill 27599-7455.
J Cardiovasc Pharmacol. 1993 Feb;21(2):264-71. doi: 10.1097/00005344-199302000-00012.
We wished to examine whether enhanced depressor baroreflexes contribute to the hypotensive effect of clonidine in rats. Clonidine's hypotensive effect and clonidine's effect on baroreflex gain mean heart rate/mean blood pressure, (delta HR/delta BP) were compared under two conditions: in conscious rats with intact baroreflex control of HR, and in pentobarbital-anesthetized (PA) rats in which baroreflex control of HR is obtunded. Clonidine produced greater hypotension and bradycardia in PA rats than in conscious rats, but this greater hypotension was not associated with enhancement of baroreflex gain. Instead, clonidine-induced hypotension in PA rats was associated with a further decrease in baroreflex gain, whereas hypotension in conscious rats was not associated with any change in baroreflex gain. Selective pharmacologic blockade of sympathetic (i.e., with atenolol treatment) or parasympathetic (i.e., with methyl-atropine treatment) control of HR showed that clonidine decreased baroreflex gain in PA rats through inhibition of sympathetic control of HR. This study suggests that clonidine's hypotensive effect is not associated with enhancement of reflex bradycardic responses in rats.
我们希望研究增强的降压压力反射是否有助于可乐定对大鼠的降压作用。在两种情况下比较了可乐定的降压作用以及可乐定对压力反射增益（平均心率/平均血压，即ΔHR/ΔBP）的影响：一种是在心率受压力反射控制完整的清醒大鼠中，另一种是在心率的压力反射控制被削弱的戊巴比妥麻醉（PA）大鼠中。可乐定在PA大鼠中比在清醒大鼠中产生更大程度的低血压和心动过缓，但这种更大程度的低血压与压力反射增益的增强无关。相反，PA大鼠中可乐定诱导的低血压与压力反射增益的进一步降低有关，而清醒大鼠中的低血压与压力反射增益的任何变化均无关。对心率的交感神经（即通过阿替洛尔治疗）或副交感神经（即通过甲基阿托品治疗）控制进行选择性药理阻断表明，可乐定通过抑制心率的交感神经控制来降低PA大鼠的压力反射增益。这项研究表明，可乐定的降压作用与大鼠反射性心动过缓反应的增强无关。
