Middlekauff H R, Nitzsche E U, Nguyen A H, Hoh C K, Gibbs G G
Department of Medicine, UCLA School of Medicine 90095, USA.
Circ Res. 1997 Jan;80(1):62-8. doi: 10.1161/01.res.80.1.62.
During static exercise, several reflex systems that increase sympathetic nerve activity, heart rate, arterial pressure, and cardiac output are activated. At rest, the renal circulation receives the most blood flow per tissue weight of any organ in the body. However, the renal circulatory response to static exercise has not been studied in humans because of technical limitations in methods for measuring rapid changes in renal blood flow. The aim of this study was to determine the renal blood flow response to static exercise in healthy humans and, specifically, to clarify the reflex mechanisms underlying this response. Renal cortical blood flow was measured using dynamic positron emission tomography and the blood flow agent oxygen-15 water. Graded handgrip exercise, posthandgrip circulatory arrest, and administration of intra-arterial adenosine were performed to clarify the mechanisms controlling renal blood flow during static exercise. The major new findings in this study are that in healthy humans (1) renal cortical blood flow decreases (basal versus handgrip, 4.4 +/- 0.1 versus 3.5 +/- 0.1 mL.min-1.g-1; P = .008) and renal cortical vascular resistance increases (basal versus handgrip, 17 +/- 1 versus 26 +/- 2 U; P = .01) in response to static handgrip exercise; (2) central command and/or the mechanoreflex contributes importantly to the early decrease in renal blood flow (basal versus handgrip, 4.2 +/- 0.2 versus 3.5 +/- 0.3 mL.min-1.g-1; P = .04) and to the increase in renal cortical vascular resistance (basal versus handgrip, 20 +/- 1 versus 25 +/- 2 U; P = .04); (3) the muscle metaboreflex contributes to further decreases in renal blood flow (basal versus posthandgrip circulatory arrest, 4.3 +/- 0.1 versus 3.5 +/- 0.2 mL.min-1.g-1; P = .002) and increases in renal cortical vascular resistance (basal versus handgrip, 18 +/- 1 versus 25 +/- 3 U; P = .002); and (4) exogenous adenosine activates the muscle metaboreflex producing reflex renal vasoconstriction and decreased renal blood flow, which may implicate endogenous adenosine generated during ischemic exercise as a potential activator of the muscle metaboreflex during ischemic handgrip exercise.
在静态运动期间，几个能增加交感神经活动、心率、动脉血压和心输出量的反射系统被激活。在静息状态下，肾循环接受的血流量在身体所有器官中按每组织重量计算是最多的。然而，由于测量肾血流量快速变化的方法存在技术限制，肾循环对静态运动的反应在人类中尚未得到研究。本研究的目的是确定健康人在静态运动时的肾血流量反应，具体而言，是阐明这种反应背后的反射机制。使用动态正电子发射断层扫描和血流剂氧 - 15水来测量肾皮质血流量。进行分级握力运动、握力后循环阻断以及动脉内注射腺苷，以阐明静态运动期间控制肾血流量的机制。本研究的主要新发现是，在健康人中：(1) 响应静态握力运动时，肾皮质血流量减少（基础状态与握力时，4.4±0.1 与 3.5±0.1 mL·min⁻¹·g⁻¹；P = 0.008），肾皮质血管阻力增加（基础状态与握力时，17±1 与 26±2 U；P = 0.01）；(2) 中枢指令和/或机械反射对肾血流量的早期减少（基础状态与握力时，4.2±0.2 与 3.5±0.3 mL·min⁻¹·g⁻¹；P = 0.04）以及肾皮质血管阻力的增加（基础状态与握力时，20±1 与 25±2 U；P = 0.04）起重要作用；(3) 肌肉代谢反射导致肾血流量进一步减少（基础状态与握力后循环阻断时，4.3±0.1 与 3.5±0.2 mL·min⁻¹·g⁻¹；P = 0.002）以及肾皮质血管阻力增加（基础状态与握力时，18±1 与 25±3 U；P = 0.002）；(4) 外源性腺苷激活肌肉代谢反射，产生反射性肾血管收缩并降低肾血流量，这可能意味着缺血运动期间产生的内源性腺苷是缺血握力运动期间肌肉代谢反射的潜在激活剂。
