Rongen G A, Senn B L, Ando S, Notarius C F, Stone J A, Floras J S
Division of Cardiology, Mount Sinai Hospital, Toronto, ON, Canada.
Can J Physiol Pharmacol. 1997 Feb;75(2):128-34.
Adenosine increases heart rate and sympathetic nerve activity reflexively in conscious humans through several mechanisms. The purpose of this study was to assess the relative contributions of arterial baroreceptor unloading, carotid chemoreceptor stimulation, and other adenosine-sensitive afferent nerves to these responses. In 12 healthy men, the effect on blood pressure, heart rate (HR), and muscle sympathetic nerve activity (MSNA; peroneal nerve) of lower body negative pressure (LBNP; -15 mmHg (1 mmHg = 133.3 Pa)) was compared with the effect of intravenous adenosine (35, 70, and l40 micrograms.kg-1.min-1). In eight subjects, the highest dose was reinfused during 100% oxygen to suppress arterial chemoreceptors. Blood pressure reductions during LBNP and adenosine (140 micrograms.kg-1.min-1) were similar. HR did not change significantly during LBNP (+2 +/- 2 beats/min; mean +/- SE) but increased at the highest adenosine dose (+25 +/- 3 beats/min; p < 0.05). MSNA increased significantly (p < 0.05) during both interventions (+255 +/- 82 and +247 +/- 58 units/100 beats for adenosine and LBNP, respectively), and there was no difference in the MSNA response to these two stimuli (p > 0.1). Oxygen inhibited adenosine-induced increases in HR and MSNA (from +305 +/- 99 to +198 +/- 75 units/100 beats and from +26 +/- 4 to +18 +/- 3 beats/min; p < 0.05 for both comparisons). The MSNA response to these combined stimuli was similar to that observed during LBNP. In contrast, the residual HR response (+18 +/- 3 beats/min) was significantly greter than the response to LBNP (+2 +/- 2 beats/min; p < 0.05). These data indicate that arterial baroreceptor unloading cannot account for the marked adenosine-induced increase in HR, but may be sufficient to explain its effect on MSNA. The effect of 100% oxygen confirms that stimulation of carotid chemoreceptors accounts for approximately one-third of the HR and MSNA response to adenosine. However, other mechanisms, such as stimulation of adenosine-sensitive afferent nerves in other vascular beds, are involved in the HR and possibly the MSNA response.
在清醒的人类中，腺苷通过多种机制反射性地增加心率和交感神经活动。本研究的目的是评估动脉压力感受器卸载、颈动脉化学感受器刺激以及其他腺苷敏感传入神经对这些反应的相对贡献。在12名健康男性中，比较了下体负压（LBNP；-15 mmHg（1 mmHg = 133.3 Pa））对血压、心率（HR）和肌肉交感神经活动（MSNA；腓总神经）的影响与静脉注射腺苷（35、70和140微克·千克⁻¹·分钟⁻¹）的影响。在8名受试者中，在100%氧气吸入期间再次输注最高剂量以抑制动脉化学感受器。LBNP和腺苷（140微克·千克⁻¹·分钟⁻¹）期间的血压降低相似。LBNP期间HR无显著变化（+2±2次/分钟；平均值±标准误），但在腺苷最高剂量时增加（+25±3次/分钟；p<0.05）。两种干预期间MSNA均显著增加（p<0.05）（腺苷和LBNP分别为+255±82和+247±58单位/100次搏动），并且对这两种刺激的MSNA反应无差异（p>0.1）。氧气抑制了腺苷诱导的HR和MSNA增加（从+305±99到+198±75单位/100次搏动，以及从+26±4到+18±3次/分钟；两种比较均p<0.05）。对这些联合刺激的MSNA反应与LBNP期间观察到的相似。相比之下，残余的HR反应（+18±3次/分钟）显著大于对LBNP的反应（+2±2次/分钟；p<0.05）。这些数据表明，动脉压力感受器卸载不能解释腺苷诱导的HR显著增加，但可能足以解释其对MSNA的影响。100%氧气的作用证实，颈动脉化学感受器刺激约占对腺苷的HR和MSNA反应的三分之一。然而，其他机制，如刺激其他血管床中的腺苷敏感传入神经，也参与了HR反应，可能还参与了MSNA反应。
