Attenuated muscle metaboreflex-induced pressor response during postexercise muscle ischemia in renovascular hypertension.

Attenuated muscle metaboreflex-induced pressor response during postexercise muscle ischemia in renovascular hypertension.
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肾血管性高血压运动后肌肉缺血期间肌肉代谢反射引起的升压反应减弱。

DOI:
10.1152/ajpregu.00464.2014
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发表时间:
2015
期刊:
American journal of physiology. Regulatory, integrative and comparative physiology
影响因子:
--
通讯作者:
O'Leary,DonalS
O'Leary,DonalS
中科院分区:
--
文献类型:
--
作者:
Spranger,MartyD;Kaur,Jasdeep;Sala-Mercado,JavierA;Machado,TiagoM;Krishnan,AbhinavC;Alvarez,Alberto;O'Leary,DonalS

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在动态运动期间,肌肉代谢反射激活(MMA;通过部分后肢缺血诱导)显著增加平均动脉压(MAP),并且当运动停止后维持缺血时MAP持续(运动后肌肉缺血,PEMI)。我们以前报道过,正常人PEMI期间的持续升压反应是由心输出量(CO)持续增加驱动的,而无外周血管收缩。然而,我们最近发现,在高血压(HTN)中,MMA引起的CO升高明显减弱。在HTN的PEMI期间维持升压反应的机制尚不清楚。在6只长期使用器械的犬中,在HTN诱导前后[Goldblatt两肾一夹(2K 1C)],观察了相同动物在休息、轻度运动(3.2 km/h)、MMA和PEMI期间的血流动力学反应。在对照组中,MAP、CO和HR随MMA升高(+52 ± 6 mmHg、+2.1 ± 0.3 l/min和+37 ± 7次/min)。诱导HTN后,静息时MAP从97 ± 3升至130 ± 4 mmHg,代谢反射反应明显减弱(+32 ± 5 mmHg,+0.6 ± 0.2 l/min和+11 ± 3 bpm)。在HTN的PEMI期间,HR和CO不持续,MAP降至正常恢复水平。我们的结论是,衰减代谢反射诱导的HR,CO和MAP的反应是不持久的PEMI在HTN。
During dynamic exercise, muscle metaboreflex activation (MMA; induced via partial hindlimb ischemia) markedly increases mean arterial pressure (MAP), and MAP is sustained when the ischemia is maintained following the cessation of exercise (postexercise muscle ischemia, PEMI). We previously reported that the sustained pressor response during PEMI in normal individuals is driven by a sustained increase in cardiac output (CO) with no peripheral vasoconstriction. However, we have recently shown that the rise in CO with MMA is significantly blunted in hypertension (HTN). The mechanisms sustaining the pressor response during PEMI in HTN are unknown. In six chronically instrumented canines, hemodynamic responses were observed during rest, mild exercise (3.2 km/h), MMA, and PEMI in the same animals before and after the induction of HTN [Goldblatt two kidney, one clip (2K1C)]. In controls, MAP, CO and HR increased with MMA (+52 ± 6 mmHg, +2.1 ± 0.3 l/min, and +37 ± 7 beats per minute). After induction of HTN, MAP at rest increased from 97 ± 3 to 130 ± 4 mmHg, and the metaboreflex responses were markedly attenuated (+32 ± 5 mmHg, +0.6 ± 0.2 l/min, and +11 ± 3 bpm). During PEMI in HTN, HR and CO were not sustained, and MAP fell to normal recovery levels. We conclude that the attenuated metaboreflex-induced HR, CO, and MAP responses are not sustained during PEMI in HTN.
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