Identification of Angiotensin II- and Kinin-Dependent Mechanisms in Essential Hypertension
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  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 . 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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- 5.Brunner HR, Gavras H, Waeber B, Kershaw GR, Turini GA, Vukovich RA, McKinstry DN, Gavras I Angiotensin-converting enzyme inhibitor in long-term treatment of hypertensive patients. Am Int Med 90: 19–23Google Scholar
- 11.Miurhead EE, Prewitt RL, Brooks jr B, Brosius jr WL (1978) Antihypertensive action of the orally active converting enzyme inhibitor (SQ 14.225) in spontaneously hypertensive rats. Circ Res Suppl I 43: I-53–I-59Google Scholar
- 12.McCaa RE, Hall JE, McCaa CS (1978) The effects of angiotensin I-converting enzyme inhibitors on arterial blood pressure and urinary sodium excretion. Role of the renal renin-angiotensin and kallikrein-kinin systems. Circ Res Suppl I 43: I-32–I-39Google Scholar