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Gene Review

Ace  -  angiotensin I converting enzyme

Rattus norvegicus

Synonyms: ACE, Angiotensin-converting enzyme, Dcp1, Dipeptidyl carboxypeptidase I, Kininase II, ...
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Disease relevance of Ace

  • On the basis of evidence suggesting the activation of the kallikrein-kinin system in steroid-induced hypertension, we considered the possibility that the angiotensin-converting enzyme inhibitor captopril would lower the arterial blood pressure in deoxycorticosterone acetate (DOCA)-salt hypertensive rats through kininase II inhibition [1].
  • Since ACE is identical to kininase II, which inactivates the nonapeptide bradykinin (BK) and related kinins, potentiation of kinins might be responsible for these additional effects of ACE inhibitors. a) In rats made hypertensive by aortic banding, the effect of ramipril in left ventricular hypertrophy (LVH) was investigated [2].
  • Ace exposure occurring concurrent with injury would augment the acute-phase response, which would augment the toxic effects of IL-1 and other cytokines, and Ace exposure occurring prior to the injury would suppress or abolish the initial stimulatory effects of IL-1, which would decrease an organism's ability to combat infection or injury [3].
  • Diverse effects of Ace inhibitors and angiotensin II receptor antagonists on prevention of cardiac hypertrophy and collagen distribution in spontaneously hypertensive rats [4].
  • Thus, tissue Met concentrations in Ace-treated rats were significantly higher than in Met-treated rats and the inhibition of AChE activity was not consistent with the amount of metabolically formed Met, supporting the hypothesis that the Ace protection plays a role in the overall toxicity [5].

Psychiatry related information on Ace

  • Presence of serotonin (5-HT) in Ace caused a rapid change of state when injected in rapid- eye-movement sleep (REM) compared with non-REM (NREM) injections [6].
  • To characterize further the neuronal activity of AMY during sleep and wakefulness, we recorded single neuronal activity in Ace across behavioral states in freely moving, normally behaving rats [7].

High impact information on Ace


Chemical compound and disease context of Ace


Biological context of Ace

  • In an F2 population [F2(S x WKY), n = 159] derived from a cross of S rats with Wistar-Kyoto (WKY) rats, Nos2 alleles did (P = 0.0070), but Ace alleles did not (P = 0.91), cosegregate with blood pressure [8].
  • Nine genetic markers, including the angiotensin-converting enzyme (Ace) and Nos2 loci spanning roughly 46 cM on rat chromosome 10, all cosegregated strongly with blood pressure in the F2(S x MNS) population [8].
  • Water intake increases with dose of dose of bradykinin, but has an inverted U-shaped relationship with dose of kininase II inhibitor [16].
  • This study therefore suggests that Ace would suppress the immune cell numbers in blood, thus decreasing an organism's immunity [3].
  • The present findings suggest that the reduction of rat sperm motility and count by Ace can be attributed to its capacity to downregulate AQP1 water channel gene expression [17].

Anatomical context of Ace

  • Thus, chronic low-level Ace exposure may impair the lineage commitment in lymphocytes, possibly by altering cytokine signaling in the brain [18].
  • Its major efferents from the central nucleus (Ace) to the basal forebrain, hypothalamus and brainstem permit it to influence sleep mechanisms [7].
  • Because serotonin introduced into AMY during REM induces short-latency changes of state, we also studied the effects of low frequency (1 Hz) electrical stimulation of the dorsal raphe nucleus (DRN) on Ace neurons [7].
  • Dex, however, did not modulate the effects of Ace and Meth on the hypothalamus, which may be attributed to the failure of Dex to modulate the CRF-gene's nGRE regulatory sites [19].
  • The endocrine effects of Ace and Met differed from their cholinergic effects, and were not proportional to the amount of Met present in different tissues obtained from the treatment groups [5].

Associations of Ace with chemical compounds

  • It was thus discovered that converting enzyme (CE) is identical with the bradykinin-degrading enzyme, kininase II, and CEIs can therefore potentiate the vasodepressor effects of bradykinin and thereby interact with the prostaglandin system [20].
  • Angiotensin converting enzyme and kininase-II-like activities in cultured valvular interstitial cells of the rat heart [21].
  • We have previously shown that peripheral injection of bradykinin in combination with the kininase II inhibitor, captopril, to rats produces a robust water intake [16].
  • We now extend this observation to another kininase II inhibitor, enalapril [16].
  • These results indicate that the antihypertensive activity of alacepril is due to the suppression of renin-angiotensin-aldosterone system and the enhancement of kallikrein-kinin-prostaglandin system through the inhibition of ACE (kininase II) activity in vivo [22].

Enzymatic interactions of Ace


Other interactions of Ace


Analytical, diagnostic and therapeutic context of Ace


  1. Kinin-mediated antihypertensive effect of captopril in deoxycorticosterone acetate-salt hypertension. Chen, K., Zhang, X., Dunham, E.W., Zimmerman, B.G. Hypertension (1996) [Pubmed]
  2. Angiotensin converting enzyme inhibitors, left ventricular hypertrophy and fibrosis. Linz, W., Wiemer, G., Schaper, J., Zimmermann, R., Nagasawa, K., Gohlke, P., Unger, T., Schölkens, B.A. Mol. Cell. Biochem. (1995) [Pubmed]
  3. Immunotoxicity of acute acephate exposure in control or IL-1-challenged rats: correlation between the immune cell composition and corticosteroid concentration in blood. Singh, A.K., Jiang, Y. Journal of applied toxicology : JAT. (2002) [Pubmed]
  4. Diverse effects of Ace inhibitors and angiotensin II receptor antagonists on prevention of cardiac hypertrophy and collagen distribution in spontaneously hypertensive rats. Gagnon, C., Legault, F., Geraldes, P., Tanguay, J.F., Lambert, C. International journal of cardiology. (2004) [Pubmed]
  5. Acute effects of acephate and methamidophos on acetylcholinesterase activity, endocrine system and amino acid concentrations in rats. Spassova, D., White, T., Singh, A.K. Comp. Biochem. Physiol. C Toxicol. Pharmacol. (2000) [Pubmed]
  6. The amygdala: a critical modulator of sensory influence on sleep. Morrison, A.R., Sanford, L.D., Ross, R.J. Biological signals and receptors. (2000) [Pubmed]
  7. Sleep-related neurons in the central nucleus of the amygdala of rats and their modulation by the dorsal raphe nucleus. Jha, S.K., Ross, R.J., Morrison, A.R. Physiol. Behav. (2005) [Pubmed]
  8. Locus for the inducible, but not a constitutive, nitric oxide synthase cosegregates with blood pressure in the Dahl salt-sensitive rat. Deng, A.Y., Rapp, J.P. J. Clin. Invest. (1995) [Pubmed]
  9. Neutral endopeptidase and kininase II mediate glucocorticoid inhibition of neurogenic inflammation in the rat trachea. Piedimonte, G., McDonald, D.M., Nadel, J.A. J. Clin. Invest. (1991) [Pubmed]
  10. Prostaglandins mediate the vasodilatory effect of mannitol in the hypoperfused rat kidney. Johnston, P.A., Bernard, D.B., Perrin, N.S., Levinsky, N.G. J. Clin. Invest. (1981) [Pubmed]
  11. Kallikrein-induced uterine contraction independent of kinin formation. Chao, J., Buse, J., Shimamoto, K., Margolius, H.S. Proc. Natl. Acad. Sci. U.S.A. (1981) [Pubmed]
  12. Insulin enhances the bradykinin response in L8 rat skeletal myoblasts. Kudoh, A., Dietze, G.J., Rabito, S.F. Diabetes (2000) [Pubmed]
  13. Substance P and capsaicin-induced mechanical hyperalgesia in the rat knee joint; the involvement of bradykinin B1 and B2 receptors. Davis, A.J., Perkins, M.N. Br. J. Pharmacol. (1996) [Pubmed]
  14. Potentiating effect of converting enzyme inhibitor captopril to the renal responses of magnesium lithospermate B in rats with adenine-induced renal failure. Yokozawa, T., Chung, H.Y., Lee, T.W., Oura, H., Nonaka, G., Nishioka, I. Chem. Pharm. Bull. (1991) [Pubmed]
  15. Attenuation of reperfusion arrhythmias by selective inhibition of angiotensin-converting enzyme/kininase II in the ischemic zone: mediated by endogenous bradykinin? Shimada, Y., Avkiran, M. J. Cardiovasc. Pharmacol. (1996) [Pubmed]
  16. Bradykinin-induced water intake and brain fos-like immunoreactivity in rats. Rowland, N.E., Fregly, M.J., Cimmerer, A.L. Brain Res. (1995) [Pubmed]
  17. Influence of acetazolamide on AQP1 gene expression in testis and on sperm count/motility in epididymis of rats. Yu, H.M., Sun, B.M., Bai, Q., Koide, S.S., Li, X.J. Arch. Androl. (2002) [Pubmed]
  18. Lipopolysaccharide (LPS) induced activation of the immune system in control rats and rats chronically exposed to a low level of the organothiophosphate insecticide, acephate. Singh, A.K., Jiang, Y. Toxicology and industrial health. (2003) [Pubmed]
  19. Acute effects of acephate and methamidophos and interleukin-1 on corticotropin-releasing factor (CRF) synthesis in and release from the hypothalamus in vitro. Singh, A.K. Comp. Biochem. Physiol. C Toxicol. Pharmacol. (2002) [Pubmed]
  20. The role of tissue renin-angiotensin systems in hypertension and effects of chronic converting-enzyme inhibition. Keuneke, C., Yacullo, R., Metzger, R., Hellmann, T., Peters, J., Ganten, D. Eur. Heart J. (1990) [Pubmed]
  21. Angiotensin converting enzyme and kininase-II-like activities in cultured valvular interstitial cells of the rat heart. Katwa, L.C., Ratajska, A., Cleutjens, J.P., Sun, Y., Zhou, G., Lee, S.J., Weber, K.T. Cardiovasc. Res. (1995) [Pubmed]
  22. Effect of alacepril on renin-angiotensin-aldosterone system and kallikrein-kinin-prostaglandin system in experimental animals. Hosoki, K., Takeyama, K., Minato, H., Fukuya, F., Kawahara, S., Kadokawa, T. Arzneimittel-Forschung. (1986) [Pubmed]
  23. The natriuretic mechanisms of neutral endopeptidase inhibitor in rats. Shimamoto, K., Ura, N., Iimura, O. Braz. J. Med. Biol. Res. (1994) [Pubmed]
  24. Age-related decline in thirst and sodium appetite in rats related to kininase II inhibition. Rowland, N.E., Del Bianco, A., Fregly, M.J. Regul. Pept. (1996) [Pubmed]
  25. Angiotensin-related induction of immediate early genes in rat brain. Rowland, N.E., Fregly, M.J., Li, B.H., Han, L. Regul. Pept. (1996) [Pubmed]
  26. NK1 receptors mediate neurogenic inflammatory increase in blood flow in rat airways. Piedimonte, G., Hoffman, J.I., Husseini, W.K., Snider, R.M., Desai, M.C., Nadel, J.A. J. Appl. Physiol. (1993) [Pubmed]
  27. Autoradiography of angiotensin-converting enzyme in fixed and unfixed rat brain using the specific enzyme inhibitor [125I]351A or a polyclonal antibody and [125I]staphylococcal protein A. Correa, F.M., Guilhaume, S.S., Saavedra, J.M. Neurosci. Lett. (1990) [Pubmed]
  28. Compensatory increase in adrenomedullary angiotensin-converting enzyme activity (kininase II) after unilateral adrenalectomy. Israel, A., Barbella, Y., Saavedra, J.M. Regul. Pept. (1986) [Pubmed]
  29. Estrogens regulate angiotensin-converting enzyme and angiotensin receptors in female rat anterior pituitary. Seltzer, A., Pinto, J.E., Viglione, P.N., Correa, F.M., Libertun, C., Tsutsumi, K., Steele, M.K., Saavedra, J.M. Neuroendocrinology (1992) [Pubmed]
  30. Direct renal action of captopril (SQ 14225): dissociation of natriuretic and vascular actions in isolated perfused rat kidney. Ogihara, T., Yasui, T., Nakane, H., Nakane, Y., Satura, T. Am. J. Cardiol. (1982) [Pubmed]
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