Young borderline hypertensive patients exhibit increased urinary kallikrein excretion and plasma renin activity, suggesting an abnormality in the interaction between the renin-angiotensin-aldosterone and kallikrein-kinin systems rather than a primary kallikrein deficiency.
Challenges prior kallikrein deficiency hypothesis in hypertension; leaves open causal role of renin-kinin interactions.
Urinary kallikrein excretion was measured in 46 young patients with borderline hypertension and 28 age-matched normotensive subjects. Hypertensives excreted greater amounts of kallikrein than normotensives (2.31 +/- 0.20 units/day vs. 1.56 +/- 0.17 units/day, p less than 0.01). Plasma renin activity (PRA) was also increased in hypertensives. Moreover, urinary kallikrein was increased in hypertensive patients with high PRA (PRA greater than or equal to mean + 1SEM in normotensives; n = 25) as compared to patients with normal PRA (PRA less than mean + 1SEM; n = 21). In hypertensives with normal PRA, urinary aldosterone correlated to urinary kallikrein (r = 0.478, p less than 0.05), as in normotensives (r = 0.451, p less than 0.02). But, no correlation was found in patients with high PRA. Therefore, the results of the present study do not confirm the hypothesis that the deficiency of the kallikrein-kinin system is the primary cause of hypertension. In hypertensives with high PRA, there may be abnormality of the interaction between the renin-angiotensin-aldosterone system and the kallikrein-kinin system, whereas it may be normal in hypertensives with normal PRA as well as normotensives.
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Ando et al. (1983) studied this question.
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