Abstract
Recently, pharmacologic tools have been used to assess the specific contributions of the renin-angiotensin system to the pathogenesis of essential hypertension [1–3]. One agent, SQ 14.225, and orally active inhibitor of the angiotensin-converting enzyme [4] has been shown to lower pressure in patients with both essential and renovascular hypertension [5–8]. It has been postulated that the blood pressure changes with converting enzyme inhibition are mediated by a fall in angiotensin II concentration [1–3]. However, interpretation of pressure responses to converting-enzyme inhibition has been complicated, since the angiotensin-converting enzyme is identical to the kininase II [9]. Therefore, the fall in blood pressure with converting enzyme inhibition could also be due to diminished degradation of bradykinin [10–12].
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Overlack, A., Stumpe, K.O., Heck, I., Ressel, C., Kühnert, M., Krück, F. (1980). Identification of Angiotensin II- and Kinin-Dependent Mechanisms in Essential Hypertension. 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_18
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DOI: https://doi.org/10.1007/978-3-642-67712-0_18
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