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(Hypertension. 2003;42:693.)
© 2003 American Heart Association, Inc.

Scientific Contributions

N-Domain Angiotensin I-Converting Enzyme With 80 kDa as a Possible Genetic Marker of Hypertension

Georgia D.M. Marques; Beata M.R. Quinto; Frida L. Plavinik; José E. Krieger; Odair Marson; Dulce E. Casarini

From Departamento de Medicina, Disciplina de Nefrologia (G.D.M.M., B.M.R.Q., F.L.P., O.M., D.E.C.), UNIFESP, Escola Paulista de Medicina, and Laboratório de Genética e Cardiologia Molecular (J.E.K.), INCOR, São Paulo, Brazil.

Correspondence to Dr Dulce Elena Casarini, Universidade Federal de São Paulo, Escola Paulista de Medicina, Depto de Medicina, Disciplina de Nefrologia, Rua Botucatu 740, CEP 04023-900, São Paulo, SP, Brazil. E-mail dulce{at}nefro.epm.br

We have previously described angiotensin I-converting enzyme (ACE) forms in urine of normotensive (190 and 65 kDa) and hypertensive patients (90 and 65 kDa, N-domain ACEs). Based on the results described above, experimental and genetic models of hypertension were investigated to distinguish hemodynamic and genetic influence on the generation of ACE profile in urine: Wistar-Kyoto and Brown Norway rats (WKY and BN), spontaneously and stroke-prone spontaneously hypertensive rats (SHR and SHR-SP), one kidney/one clip rats (1K1C), deoxycorticosterone acetate (DOCA) salt-treated and untreated rats, and enalapril-treated SHR (SHRen). Two peaks with ACE activity were separated from the urine of WKY and BN rats submitted to an AcA-44 column, WK-1/BN-1 (190 kDa), and WK-2/BN-2 (65 kDa), as described for urine of normotensive subjects. The same results were obtained for urine of 1K1C and DOCA salt-treated and untreated rats, analyzed to evaluate the influence of hemodynamic factors in the ACE profile in urine. The urine from SHR, SHR-SP, and SHRen presented 80 (S-1, SP-1, Sen-1) and 65 (S-2, SP-2, Sen-2) kDa ACE forms, differing from the urine profile of normotensive rats, but similar to that described for hypertensive patients. The presence of 80 kDa ACE in urine of SHR, SHR-SP, and SHRen and its absence in urine of experimental hypertensive rats (1K1C and DOCA salt) support the hypothesis that this enzyme could be a possible genetic marker of hypertension. Taken together, our results provide evidence that ACE forms with 90/80 kDa isolated from the urine of hypertensive subjects and genetic hypertensive animals behaves as a possible genetic marker of hypertension and not as a marker of high blood pressure.

Key Words: angiotensin-converting enzyme • genetics • hypertension, genetic

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