Taneyama C, Goto H, Benson K T, Unruh G K, Arakawa K
Department of Anesthesiology, University of Kansas Medical Center, Kansas City 66103.
Anesth Analg. 1991 Mar;72(3):351-8. doi: 10.1213/00000539-199103000-00012.
The reason why adenine compounds when used as hypotensive agents are devoid of significant reflex sympathetic activity, such as rebound hypertension and tachycardia, is not clearly understood. This study, performed on alpha-chloralose-anesthetized dogs, examined, first, the effects of adenosine triphosphate (ATP) and adenosine as compared with those of sodium nitroprusside on efferent renal sympathetic nerve activity (RSNA), as an indicator of general reflex sympathetic activity, and second, whether vagal involvement could be demonstrated in the action of ATP and adenosine on RSNA. Renal sympathetic nerve activity increased progressively with increasing doses of sodium nitroprusside (5, 10, and 20 micrograms/kg) and adenosine (0.5, 2.0, and 4.0 mg/kg), whereas ATP suppressed RSNA at 2.0 and 4.0 mg/kg. High doses of ATP and adenosine (4.0 mg/kg) were injected into intact (n = 7) and vagotomized dogs (n = 7). Both ATP and adenosine induced rapid onset of hypotension without rebound hypertension and tachycardia. After vagotomy, the attenuation of RSNA by ATP was completely abolished and rebound hypertension and tachycardia were observed. Vagotomy did not alter the effect of adenosine on RSNA. It is concluded that ATP-induced hypotension is associated with attenuation of sympathetic efferent nerve activity mediated through vagal afferent pathways. Vagal afferent impulses are thought to be one of the mechanisms that inhibit reflex sympathetic activities, such as rebound hypertension after ATP-induced hypotension. The mechanisms by which adenosine inhibits reflex sympathetic activity are not, however, secondary to vagal afferent involvement and must be multifactorial.
当腺嘌呤化合物用作降压药时，为何没有明显的反射性交感神经活动，如反弹性高血压和心动过速，目前尚不清楚。本研究在α-氯醛糖麻醉的犬身上进行，首先，将三磷酸腺苷（ATP）和腺苷与硝普钠对传出肾交感神经活动（RSNA）的影响进行比较，RSNA作为一般反射性交感神经活动的指标；其次，研究ATP和腺苷对RSNA的作用中是否能证明迷走神经的参与。随着硝普钠（5、10和20微克/千克）和腺苷（0.5、2.0和4.0毫克/千克）剂量的增加，肾交感神经活动逐渐增加，而ATP在2.0和4.0毫克/千克时抑制RSNA。将高剂量的ATP和腺苷（4.0毫克/千克）注入完整犬（n = 7）和迷走神经切断犬（n = 7）体内。ATP和腺苷均迅速引起低血压，且无反弹性高血压和心动过速。迷走神经切断后，ATP对RSNA的减弱作用完全消失，并观察到反弹性高血压和心动过速。迷走神经切断未改变腺苷对RSNA的作用。得出的结论是，ATP诱导的低血压与通过迷走神经传入途径介导的交感神经传出神经活动减弱有关。迷走神经传入冲动被认为是抑制反射性交感神经活动的机制之一，如ATP诱导低血压后的反弹性高血压。然而，腺苷抑制反射性交感神经活动的机制并非继发于迷走神经传入参与，而必定是多因素的。
