REDUCED URINARY KALLIKREIN EXCRETION IN HUMAN RENOVASCULAR HYPERTENSION CAUSED BY NONSPECIFIC AORTOARTERITIS AND OTHER DISORDERS

In this study urinary kallikrein excretion was measured using the kini nogenase bioassay technique in 12 normal volunteers and 23 patients wi th angiographically-proven renovascular hypertension (RVHT). In 13 of these (group I), RVHT was due to nonspecific aortoarteritis (NSAA) and in 10 (group II) due to other causes. Urinary kallikrein (UKa) excret ion was significantly lower in patients, with values still lower in NS AA. PRA was high in both the groups in comparison with controls; howev er, the levels were significantly lower in group I compared with group II. Finding of both UKa and PRA lower in group I is suggestive of lon g standing hypertension becoming volume dependent with nephrosclerotic changes in the kidney. These results point to decreased renal kallikr ein-kinin system activity as a feature of NSAA that probably contribut es chiefly to the maintenance of the hypertensive state. Normalisation of BP with restoration of UKa and PRA towards normal in three patient s of group I and five in group II further support the role of UKa not only when over activity of renin-angiotensin system is responsible for RVHT as in group II but also in group I when the hypertension becomes volume dependent.