Sakai T, Ideishi M, Miura S, Maeda H, Tashiro E, Koga M, Kinoshita A, Sasaguri M, Tanaka H, Shindo M, Arakawa K
Department of Internal Medicine, School of Medicine, Fukuoka University, Japan.
J Hum Hypertens. 1998 Jun;12(6):355-62. doi: 10.1038/sj.jhh.1000608.
The role of renal dopamine in the early depressor effect of exercise was evaluated in hypertensives.
After a general clinical observation period of 4 weeks, 29 essential hypertensives were divided into two groups. The exercise group (n=16) underwent blood lactate threshold exercise using a cycle ergometer for 60 min three times a week for 4 weeks.
In the non-exercise group (n=13), blood pressure (BP) and humoral variables did not change significantly (from 150+/-3/93+/-2 to 145+/-2/94+/-1 mm Hg). In the exercise group (n=16), resting BP was significantly reduced from 158+/-2/92+/-2 at week 0 to 145+/-3/85+/-3 mm Hg at week 4. The increase in urinary free dopamine excretion (from 248+/-14 to 276+/-24 ng/mg Cr) at week 4 was significantly higher than that in the non-exercise group (from 220+/-31 to 196+/-27 ng/mg Cr). In the exercise group, urinary kallikrein activity also increased significantly from 173.0+/-35.4 at week 0 to 320.3+/-63.3 ng bradykinin/min/mg Cr at week 4. These changes in urinary free dopamine excretion and urinary kallikrein activity were negatively correlated with the change in BP. The change in urinary sodium excretion was also negatively correlated with the change in plasma volume index. Moreover, the change in urinary free dopamine excretion was positively correlated with the changes in urinary kallikrein activity and urinary sodium excretion. The change in renal decarboxylation rate of DOPA (3,4-dihydroxyphenylalanine) positively correlated with the changes in urinary free dopamine excretion and urinary sodium excretion, and was negatively correlated with the change in systolic BP.
These results suggest that exercise triggered renal dopamine generation and activation of renal kallikrein-kinin system, resulting in natriuresis and BP reduction in the early phase (4 weeks) of mild exercise.
评估肾多巴胺在高血压患者运动早期降压效应中的作用。
经过4周的一般临床观察期后，29例原发性高血压患者被分为两组。运动组（n = 16）使用自行车测力计进行血乳酸阈值运动，每周3次，每次60分钟，共4周。
在非运动组（n = 13）中，血压（BP）和体液变量无显著变化（从150±3/93±2降至145±2/94±1 mmHg）。在运动组（n = 16）中，静息血压从第0周的158±2/92±2显著降至第4周的145±3/85±3 mmHg。第4周时尿游离多巴胺排泄量增加（从248±14增至276±24 ng/mg Cr），显著高于非运动组（从220±31降至196±27 ng/mg Cr）。在运动组中，尿激肽释放酶活性也从第0周的173.0±35.4显著增至第4周的320.3±63.3 ng缓激肽/分钟/mg Cr。尿游离多巴胺排泄量和尿激肽释放酶活性的这些变化与血压变化呈负相关。尿钠排泄量的变化也与血浆容量指数的变化呈负相关。此外，尿游离多巴胺排泄量的变化与尿激肽释放酶活性和尿钠排泄量的变化呈正相关。多巴（3,4 - 二羟基苯丙氨酸）的肾脱羧率变化与尿游离多巴胺排泄量和尿钠排泄量的变化呈正相关，与收缩压变化呈负相关。
这些结果表明，运动触发肾多巴胺生成并激活肾激肽释放酶 - 激肽系统，导致轻度运动早期（4周）出现利钠和血压降低。
