Urinary kallikrein activity was significantly lower in hypertensive compared to normotensive white men and correlated directly with renal blood flow, suggesting a role for the kallikrein-kinin system in regulating renal vascular resistance.
Cross-Sectional (n=59)
No
Does dietary sodium restriction alter urinary kallikrein activity and renal blood flow in normotensive and hypertensive black and white men?
The kallikrein-kinin and renin-angiotensin systems contribute to renal blood flow regulation and may account for racial differences in renal vascular resistance in hypertension.
Absolute Event Rate: 9.2% vs 18.7%
p-value: p=<0.025
We investigated the relationship of the kallikrein-kinin system and the renin-angiotensin system in the regulation of blood pressure, salt and water excretion, and renal blood flow. Normotensive and hypertensive black and white men were studied during unresticted sodium intake as well as on a 10-meq/day sodium intake; potassium intake was held constant throughout the study (80 meq/day). During unrestricted sodium intake, urinary kallikrein activity was greater in white normotensives than white hypertensives or black normotensives. There was no difference (P greater than 0.05) between white and black hypertensives or between black normotensives and black hypertensives. All groups had greater urinary kallikrein activity on low sodium vs. unrestricted sodium intake, but the increase in black hypertensives was small, and they excreted significantly less kallikrein than the ogher groups on the low sodium diet. Plasma renin activity showed similar increments after sodium restriction in all groups. Urinary kallikrein activity correlated with renal blood flow in all groups except the black normotensives on low sodium intake. Renal blood flow could be correlated uniformly with log (urinary kallikrein activity/supine plasma renin activity) in all groups on either diet. Urinary sodium and potassium excretion and urine volume were not different among the groups. We conclude: (a) important racial differences exist in urinary kallikrein activity that are unrelated to sodium or potassium excretion or urine volume; (b) dietary sodium restriction further delineates racial differences and suggests alternative pathophysiologic mechanisms for huma hypertension; (c) urinary kallikrein activity correlates with renal blood flow; and (d) our data support the concept that the kallikrein-kinin system and the renin-angiotensin system contribute to the regulation of renal blood flow and may account for racial differences in renal vascular resistance.
Levy等人（星期五）在原发性高血压患者中进行了横断面研究（n=59）。在白人男性中，评估了原发性高血压与正常血压对照组在不限制钠摄入的情况下的24小时尿激肽活性（EU/24h）（p=<0.025）。高血压患者的尿激肽活性明显低于正常血压的白人男性，并且与肾脏血流直接相关，这表明激肽-激肽系统在调节肾血管阻力中发挥了作用。