We tested the hypothesis that brief static contraction of the triceps surae muscle causes reflex-induced increases in plasma arginine vasopressin (AVP) in anesthetized cats. Arterial blood samples, for measurement of plasma AVP, were taken before and after 30 s of electrically stimulated static contraction performed at a low intensity (<20% of maximal; n = 5), a high intensity (>70% of maximal; n = 7), and a high intensity after denervation of the triceps surae (n = 5). The low intensity contraction protocol was repeated during alpha-adrenergic blockade (n = 7) to minimize potential baroreflex-induced inhibition of AVP release. Passive stretch of the triceps surae was conducted (n = 5) to determine effects of muscle mechanoreceptor stimulation on the release of AVP. Low intensity contraction had no effect on plasma AVP. During alpha-adrenergic blockade, this same contraction intensity caused this peptide to increase from 12.8 +/- 2.1 to 17.7 +/- 2.6 pg/ml. High intensity contraction caused an increase in AVP (13.2 +/- 3.5 to 26.1 +/- 6.6 pg/ml) that was abolished by denervation (14.4 +/- 3. 7 vs. 17.1 +/- 6.6 pg/ml). Passive stretch had no effect on plasma AVP. These findings suggest that brief static contraction causes increases in plasma AVP that are reflex in nature, intensity dependent, opposed by the arterial baroreflex, and probably unrelated to muscle mechanoreceptor activation.

译文

:我们测试了以下假设:麻醉的猫,肱三头肌的短暂静态收缩会导致反射引起的血浆精氨酸加压素(AVP)升高。在以低强度(<最大值的20%; n = 5),以高强度(最大值的> 70%; n)进行电刺激的静态收缩30 s之前和之后,采集动脉血样本以测量血浆AVP。 = 7),并且在肱三头肌肱神经去神经后强度很高(n = 5)。在α-肾上腺素能阻滞(n = 7)期间重复低强度收缩方案,以使潜在的压力反射诱发的对AVP释放的抑制作用最小化。进行三头肌肱三头肌的被动拉伸(n = 5)以确定肌肉机械感受器刺激对AVP释放的影响。低强度收缩对血浆AVP没有影响。在α-肾上腺素阻断期间,相同的收缩强度导致该肽从12.8 /-2.1增加至17.7 /-2.6 pg / ml。高强度收缩导致AVP增加(13.2 /-3.5至26.1 /-6.6 pg / ml),而被去神经支配(14.4 /-3. 7 vs. 17.1 /-6.6 pg / ml)取消。被动拉伸对血浆AVP没有影响。这些发现表明,短暂的静态收缩会导致血浆AVP的增加,而血浆AVP的性质是反射性的,强度依赖性的,与动脉压力反射相反的,并且可能与肌肉机械感受器的激活无关。

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