Widdop R E, Verberne A J, Louis W J, Jarrott B
University of Melbourne, Department of Medicine, Austin Hospital, Heidelberg, Victoria, Australia.
Eur J Pharmacol. 1990 Sep 4;186(1):17-28. doi: 10.1016/0014-2999(90)94056-4.
The effect of ketanserin (3 mg/kg i.v.) on the baroreceptor heart rate reflex and the Bezold-Jarisch reflex was examined in conscious Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR). In the control situation (before ketanserin treatment), reflex bradycardia in response to phenylephrine (baroreflex) and phenyldiguanide (Bezold-Jarisch reflex) were impaired in SHR as compared with WKY, while reflex tachycardia in response to nitroprusside was similar in the two groups. However, after ketanserin administration in SHR, there was a reversal of the baroreflex-mediated tachycardia in response to nitroprusside into a bradycardic response. The nitroprusside-induced bradycardia was not caused by the release of 5-HT stimulating chemosensitive vagal afferents since the 5-HT3 receptor antagonist MDL 72222 did not block this response. In the same SHR, the Bezold-Jarisch reflex evoked by phenyldiguanide and the phenylephrine-induced bradycardia were potentiated by ketanserin. All the above effects of ketanserin were less evident in the WKY. Ketanserin did not alter vagal efferent function in anaesthetized SHR since it did not affect bradycardia induced by electrical stimulation of the vagus nerve. Therefore, it is suggested that ketanserin has sensitised cardiac vagal afferent mechanisms in SHR, which led to a normalization of reflex bradycardic function to a level normally observed in conscious normotensive WKY (i.e. prior to ketanserin treatment).
在清醒的Wistar-Kyoto大鼠（WKY）和自发性高血压大鼠（SHR）中，研究了酮色林（静脉注射3mg/kg）对压力感受器心率反射和贝佐尔德-贾里什反射的影响。在对照情况下（酮色林治疗前），与WKY相比，SHR中对去氧肾上腺素（压力反射）和苯二胍（贝佐尔德-贾里什反射）的反射性心动过缓受损，而两组对硝普钠的反射性心动过速相似。然而，在SHR中给予酮色林后，对硝普钠的压力反射介导的心动过速逆转成了心动过缓反应。硝普钠诱导的心动过缓不是由5-羟色胺释放刺激化学敏感迷走神经传入引起的，因为5-羟色胺3受体拮抗剂MDL 72222不能阻断这种反应。在同一SHR中，苯二胍诱发的贝佐尔德-贾里什反射和去氧肾上腺素诱导的心动过缓被酮色林增强。酮色林的所有上述作用在WKY中不太明显。酮色林不改变麻醉的SHR中的迷走神经传出功能，因为它不影响电刺激迷走神经诱导的心动过缓。因此，提示酮色林使SHR中的心脏迷走神经传入机制敏感化，这导致反射性心动过缓功能恢复正常，达到清醒正常血压WKY（即酮色林治疗前）通常观察到的水平。
