腺苷对颈动脉窦压力感受器反射的易化作用

在27只隔离灌流颈动脉窦区的麻醉大鼠,观察了腺苷（adenosine,Ado）对颈动脉窦压力感受器反射的影响。所得结果如下：（1）以 Ado（125μmol／L）隔离灌流大鼠左侧颈动脉窦区时,压力感受器机能曲线向左下方移位,曲线最大斜率（PS）由0．37±0．02增至0 55±0．02kPa／KPa（P＜0．001）,反射性血压下降幅度（RD）由5．53±0．12增至7．76±0．36KPa;阈压（TP）、平衡压（EP）和饱和压（SP）则分别从8．60±0．27,12．53±0．30和23．69±0．15下降至5．63± 0．11kPa,10．89±0．29KPa和20．18±0．55KPa（P＜0．01－0．001 ）。其中RD,PS和TP的变化呈明显的剂量依赖性。（2）用腺苷选择性 A1受体拮抗剂（8－cyclopentyl－l,3－dipropylianthene,0．134mmol／L）预处理后,Ado的上述反射效应即被阻断。（3）先给予KATP通道阻断剂格列苯脲（glibenclamide．10μmol／L）亦可取消腺苷对压力感受器反射的影响。以上结果表明, Ado对大鼠颈动脉窦压力感受器活动有易化作用,这一作用似与腺苷A1受体介导的KATP通道开放有关。

Adenosine facilitates carotid baroreflex in rats

The effects of adenosine (Ado) on the carotid baroreflex were studied in 27 anesthetized rats with isolated carotid sinus perfusion. The results obtained were as follows: (1) By perfusing the isolated carotid sinus with adenosine (125 mumol/L), the functional curve of baroreflex was shifted to the left and downward, with the peak slope (PS) increased from 0.37 +/- 0.02 to 0.55 +/- 0.02 kPa/kPa (P < 0.001) and the reflex decrease in mean arterial pressure (RD) enhanced from 5.53 +/- 0.12 to 7.76 +/- 0.36 kPa (P < 0.001). Meanwhile, the threshold pressure (TP), equilibrium pressure (EP) and saturation pressure (SP) were significantly decreased from 8.60 +/- 0.27 to 5.63 +/- 0.11 kPa (P < 0.001), 12.53 +/- 0.30 to 10.89 +/- 0.29 kPa (P < 0.01) and 23.69 +/- 0.15 to 20.18 +/- 0.55 kPa (P < 0.001), respectively. Among the functional parameters of carotid baroreflex, the changes of RD, PS and TP induced by Ado were dose-dependent. (2) By pretreatment with (8-cyclopentyl-1, 3-dipropylxanthine, 0.134 mmol/L), a selective adenosine A1-receptor antagonist, the above effects of Ado on carotid baroreflex were abolished. (3) The Ado-induced changes of baroreflex were also eliminated as the carotid sinus was pretreated with KATP channel blocker glibenclamide (10 mumol/L). The results strongly suggest that the carotid baroreflex could be facilitated by Ado. It is proposed that the facilitatory action of Ado on carotid baroreflex may be resulted from the opening of KATP channels mediated by Ado A1-receptors.