Abstract
To the Editor: Mitas et al., in their report in the July 27 issue of the Journal, found subnormal urinary kallikrein excretion in white male subjects with essential hypertension or hypertension secondary to renal disease of various causes. They suggested that a deficiency of the (putative vasodilator) kallikrein-kinin system could cause hypertension. However, one could argue that the lower urinary kallikrein values found in their hypertensive patients were secondary to differences between groups in renin-aldosterone activity and renal blood flow. The authors acknowledge the relation between urinary kallikrein excretion and sodium-retaining steroid activity.12 Yet they chose hypertensive patients with.
| Original language | English |
|---|---|
| Pages (from-to) | 1316-1317 |
| Number of pages | 2 |
| Journal | New England Journal of Medicine |
| Volume | 299 |
| Issue number | 23 |
| DOIs | |
| State | Published - Dec 7 1978 |
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