心室内注射腺苷对肾交感神经传出活动的影响

EFFECTS OF INTRAVENTRICULAR INJECTION OF ADENOSINE ON RENAL SYMPATHETIC NERVE ACTIVITY

在切断两侧缓冲神经和迷走神经的麻醉大鼠，观察心室内注射腺苷及其同系物对肾交感神经传出活动的影响。心室内冲击注射腺昔（0．5μmol／kg，0．1ml）时，肾交感神经传出放电（RSNA）增加41．9±6．08％（P＜0．001），并引起平均动脉血压（MAP）先短暂升高1．39±0．19kPS（P＜0．001）和随后下降3．74±0．64kPa（P＜0．001），以及心率（HR）减慢95±14bpm（P＜0．001）。为了确定何种受体亚型介导腺苷所致RSNA增加，又分别应用了选择性腺昔A1受体激动剂[（-）-N6－（2－Phenylisopropyl）adenosine，R－PIA]和A2受体激动剂[5＇－（N－ethylcarboxamido）adenosine，NECA]。无论R－PIA（0．05μmol／kg，0．1ml）或NECA（0．05μmol／kg，0．1ml）均使MAP下降和HR减慢，且作用持续时间较腺苷的明显延长；R－PIA使RSNA增加31．6±5．21％（P＜0．001），但NECA对RSNA无明显影响。选择性腺苷A1受体拮抗剂（8－cyclopentyl－1，3－dipropylxanthine，DPCPX）可完全抑制腺苷对RSNA的兴奋效应。切除双侧星状神经节后，腺苷兴奋RSNA的效应消失。以上结果提示，腺苷可通过A1受体激活心交感神经传入纤维，反射地增强肾交感神经的传出活动。

The effects of intraventricular injection of adenosine and its analogues on renalsympathetic nerve activity (RSNA) were examined in sinoaortic denervated and vagotomized anesthetized rats. In response to intraventticular bolus injection of adenosine,RSNA was increased by 41. 9± 6. 08% (P＜0. 001 ), mean arterial Ptessure (MAP)was initially increased by 1. 39± 0. 19 kPa (P＜0. 001 ) and subsequently decreasedby 3. 74± 0. 64 kPa (P＜0．001 ),and heart rate (HR) was reduced by 95±14 bpm(P＜0. 001 ). To determine the adenosine-receptor subtype which mediates the response of RSNA to adenosine,we used selective A1-receptor agonist (R-PIA) and A2-receptor agonist (NECA) and found that MAP and HR were reduced by R-PIA andNECA. The effects lasted significantly longer than those of adenosine. R-PIA inducedan increase in RSNA by 31. 6± 5. 21% (P＜0. 001 ), while NECA showed no effect onRSNA. The renal sympathoexcitatory response to intraventricular injection of adenosine was completely inhibited by pretreatment with a selective A1-receptor antugonist(DPCPX). Following the bilateral stellate ganglionectomy, intraventricular injection ofadenosine failed to induce the increase in RSNA. The results indicate that adenosinemay activate cardiac sympathetic afferents through A1-receptor, resulting in a reflexaugmentation of RSNA.