Advertisement

Identification of Angiotensin II- and Kinin-Dependent Mechanisms in Essential Hypertension

  • A. Overlack
  • K. O. Stumpe
  • I. Heck
  • C. Ressel
  • M. Kühnert
  • F. Krück
Part of the International Boehringer Mannheim Symposia book series (BOEHRINGER)

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].

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    Case DB, WaUaee JM, Keim HJ, Weber MA, Drayer JIM, White RP, Sealey JE, Laragh JH (1976) Estimating renin participation in hypertension: Superiority of converting enzyme inhibitor over saralasin. Am J Med 61: 790–796PubMedCrossRefGoogle Scholar
  2. 2.
    Case DB, Wallace JM, Keim HJ, Weber MA, Sealey JE, Laragh JH (1977) Possible role of renin in hypertension as suggested by renin-sodium profiling and inhibition of converting-enzyme. N Engl J Med 296: 641–646PubMedCrossRefGoogle Scholar
  3. 3.
    Gavras H, Brunner HR, Laragh JH, Sealey JE, Gavras I, Vukovich RA (1974) An angiotensin converting-enzyme inhibitor to identify and treat vascoconstrictor and volume factors in hypertensive patients. N Engl J Med 291: 817–821PubMedCrossRefGoogle Scholar
  4. 4.
    Gushman DW, Cheung HS, Sabo EF, Ondetti MA (1977) Design of potent competitive inhibitors of angiotensin-converting enzyme. Carboxyalkanoyl and mercaptoalkanoyl amino acids. Biochemistry 16: 5484–5491CrossRefGoogle Scholar
  5. 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
  6. 6.
    Cody jr RJ, Tarazi RC, Bravo EL, Fonad FM (1978) Haemodynamics of orally-active converting enzyme inhibitor (SQ 14.225) in hypertensive patients. Clin Sci Mol Med 55: 453–459PubMedGoogle Scholar
  7. 7.
    Ferguson RK, Brunner HR, Turini GA, Gavras H, McKinstry DN (1977) A specific orally active inhibitor of angiotensin-converting enzyme in man. Lancet 1: 775PubMedCrossRefGoogle Scholar
  8. 8.
    Gavras H, Brunner HR, Turini GA, Kershaw GR, Tifft CP, Cuttelod S, Gavras I, Vukovich RA, McKinstry DN (1978) Antihypertensive effect of the oral angiotensin converting-enzyme inhibitor SQ 14.225 in man. N Engl J Med 298: 991–995PubMedCrossRefGoogle Scholar
  9. 9.
    Erdös EG (1977) The angiotensin I converting enzyme. Fed Proc 36: 1760–1765PubMedGoogle Scholar
  10. 10.
    Williams GH, Hollenberg NK (1977) Accentuated vascular and endocrine response to SQ 20881 in hypertension. N Engl J Med 297: 184–188PubMedCrossRefGoogle Scholar
  11. 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. 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
  13. 13.
    Derkx FHM, Bouma BN, Schalekamp MPA, Schalekamp MADH (1979) An intrinsic factor XII-prekallikrein-dependent pathway activates the human plasma renin-angiotensin system. Nature 280: 315–316PubMedCrossRefGoogle Scholar
  14. 14.
    Sealey JE, Atlas SA, Laragh JH, Oza NB, Ryan JW (1978) Human urinary kallikrein converts inactive to active renin and is a possible physiological activator of renin. Nature 275: 144–145PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 1980

Authors and Affiliations

  • A. Overlack
  • K. O. Stumpe
  • I. Heck
  • C. Ressel
  • M. Kühnert
  • F. Krück

There are no affiliations available

Personalised recommendations