Changes in renal sympathetic nerve activity, heart rate and arterial blood pressure associated with eating in cats.
Changes in renal sympathetic nerve activity, heart rate and arterial blood pressure associated with eating in cats.
复制标题
与猫进食相关的肾交感神经活动、心率和动脉血压的变化。
DOI：
10.1113/jphysiol.1987.sp016696
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发表时间：
1987
期刊：
影响因子：
--
通讯作者：
I. Ninomiya
中科院分区：
文献类型：
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作者：
K. Matsukawa;I. Ninomiya
1.在进食前、进食期间和进食后，同时测量13只清醒猫的肾交感神经活动、心率和动脉血压，通过提供食物10 - 15 s的时间来诱发。2.在205次试验中，93%（191次）出现进食行为，191次试验中65%的肾交感神经活动显著增加。另一方面，在许多食物呈现试验中，当没有进食发生时，或者呈现空的食物盒时，肾交感神经活动没有显著变化。3.在食物展示后1 - 8秒开始进食。肾交感神经活动的增加与进食的开始密切相关，但与食物呈现的开始无关。肾交感神经活动和心率增加，从进食开始有0.5 - 1.5 s的轻微时滞，而动脉血压增加则在进食开始后5.5 s。开始进食后，肾交感神经活动、心率和动脉血压最多增加61 +/-18%（平均值+/-S.E.）。在1.0、5.5和11.5 s时，与对照值相比，分别为26 +/-4.0次/min和17 +/-4.9 mmHg。4.在休息时观察到的肾交感神经活动的心脏相关分组放电在进食期间增加。5.当去甲肾上腺素（2 - 5微克/千克静脉注射）升高动脉血压时，在休息期间肾交感神经活性几乎被完全抑制，并且在进食期间肾交感神经活性的增加没有被诱导。6.我们得出结论，肾交感神经活动增加与进食行为相关，但与食物呈现无关，并且肾交感神经活动的增加是由来自高级中枢神经系统的下行输入引起的，而不是由食物摄入引起的内脏自主神经反射或动脉血压降低引起的压力反射引起的。
1. Renal sympathetic nerve activity, heart rate and arterial blood pressure were simultaneously measured in thirteen awake cats before, during and after eating which was evoked by presenting food for a period of 10‐15 s. 2. With food presentation, eating behaviour occurred in 93% (191) of 205 trials, and renal sympathetic nerve activity significantly increased in 65% of the 191 trials. On the other hand, in many of food presentation trials when no eating occurred, or with presentation of an empty food box, renal sympathetic nerve activity did not change significantly. 3. Eating started 1‐8 s after the food presentation. The increase in renal sympathetic nerve activity was closely related to the beginning of eating but not to the onset of food presentation. Renal sympathetic nerve activity and heart rate increased with a slight time lag of 0.5‐1.5 s from the onset of eating, whereas an increase in arterial blood pressure followed the onset of eating by 5.5 s. After the beginning of eating, renal sympathetic nerve activity, heart rate and arterial blood pressure increased at a maximum of 61 +/‐ 18% (mean +/‐ S.E. of mean), 26 +/‐ 4.0 beats/min, and 17 +/‐ 4.9 mmHg from the control values at 1.0, 5.5 and 11.5 s, respectively. 4. Cardiac‐related grouped discharges of renal sympathetic nerve activity, which were observed at rest, increased during eating. 5. When arterial blood pressure was elevated by noradrenaline (2‐5 micrograms/kg I.V.), renal sympathetic nerve activity during resting was almost completely inhibited and the increase in renal sympathetic nerve activity during eating was not induced. 6. We conclude that renal sympathetic nerve activity increases in association with eating behaviour but not as firmly with the food presentation, and that the increase in renal sympathetic nerve activity is initiated by descending input from the higher central nervous system rather than either by the viscero‐autonomic reflex due to food intake or by the baroreflex due to a decrease in arterial blood pressure.