Abstract
There are several lines of evidence that the renal kallikrein-kinin system (KKS) is altered in various forms of hypertension, probably indicating a defective vasodepressor system as a pathogenetic factor in blood pressure regulation. Urinary kallikrein excretion was found to be decreased in patients with essential [9, 15, 18, 19, 35], renovascular [13] and renoparenchymal hypertension [25, 27] and elevated in primary aldosteronism [18, 27]. Furthermore, a dependence of the activity of the renal KKS on factors involved in the pathogenesis of hypertension (extracellular volume [21], sodium- and potassium balance [1, 10, 19, 22, 26, 36], and mineralocorticoids [19]), was established.
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Röckel, A., Stürmer, G., Schmid, G., Heidland, A. (1980). Enhanced Parotid Kallikrein Secretion in Essential, Adrenal Hypertension and in Advanced Renal Failure — Inverse Relationship to Sodium Excretion. In: Philipp, T., Distler, A. (eds) Hypertension: Mechanisms and Management. International Boehringer Mannheim Symposia. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-67712-0_17
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DOI: https://doi.org/10.1007/978-3-642-67712-0_17
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