Abnormalities of the extracellular degradation of collagen type I in essential hypertension

BACKGROUND: This study was designed to investigate whether collagen type I degradation is altered in patients with essential hypertension and whether this alteration could be related to disturbances in the serum matrix metalloproteinase pathway of collagen degradation. A second aim of the study was...

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Autores: Laviades, C. (Concepción)|||/items/488d1dd5-a5f9-4ae5-98c6-09329cae31b4, Varo-Cenarruzabeitia, N. (Nerea)|||/items/18b5a757-44b9-4e23-8a8c-ad907969001f, Fernandez, J. (Javier)|||/items/60cfb594-0850-42a3-97ae-4b29abfd6b56, Mayor, G. (Gaspar)|||/items/13bce2d0-fb4d-4db5-abe9-aef28baae51d, Gil, M.J. (María José)|||/items/ab59091b-9346-4377-8462-bfa48090ba46, Monreal, J.I. (José Ignacio)|||/items/54707c2a-e68a-4e73-9141-0276a5bc7a2b, Diez-Martinez, J. (Javier)|||/items/4f3a0e43-12bf-403d-9dc7-31fab0d11d41
Tipo de recurso: artículo
Fecha de publicación:1998
País:España
Institución:Universidad de Navarra
Repositorio:Dadun. Depósito Académico Digital de la Universidad de Navarra
Idioma:inglés
OAI Identifier:oai:dadun.unav.edu:10171/20102
Acceso en línea:https://hdl.handle.net/10171/20102
Access Level:acceso abierto
Palabra clave:Collagen
Hypertension
Metalloproteinases
Peptides
Remodeling
Descripción
Sumario:BACKGROUND: This study was designed to investigate whether collagen type I degradation is altered in patients with essential hypertension and whether this alteration could be related to disturbances in the serum matrix metalloproteinase pathway of collagen degradation. A second aim of the study was to assess whether some relation exists between serum markers of collagen type I degradation and left ventricular hypertrophy in hypertensive patients. METHODS AND RESULTS: We measured serum concentrations of carboxy-terminal telopeptide of collagen type I (CITP) as a marker of extracellular collagen type I degradation, of total matrix metalloproteinase-1 (MMP-1), or collagenase, of total tissue inhibitor of metalloproteinases 1 (TIMP-1), and of MMP-1/TIMP-1 complex in 37 patients with never-treated essential hypertension and in 23 normotensive control subjects. Serum concentrations of free MMP-1 and free TIMP-1 were calculated by subtracting the values of MMP-1/TIMP-1 complex from the values of total MMP-1 and total TIMP-1, respectively. Measurements were repeated in 26 hypertensive patients after 1 year of treatment with the ACE inhibitor lisinopril. Baseline free MMP-1 was decreased (P<0.001) and baseline free TIMP-1 was increased (P<0.001) in hypertensives compared with normotensives. No significant differences were observed in the baseline values of CITP between the 2 groups of subjects. Hypertensive patients with baseline left ventricular hypertrophy exhibited lower values of free MMP-1 (P<0.01) and CITP (P<0.05) and higher (P<0.001) values of free TIMP-1 than hypertensive patients without baseline left ventricular hypertrophy. Treated patients attained an increase (P<0.001) in free MMP-1 and a decrease (P<0.05) in free TIMP-1. In addition, serum CITP was increased (P<0.05) in treated hypertensives compared with normotensive subjects. CONCLUSIONS: These findings suggest that systemic extracellular degradation of collagen type I is depressed in patients with essential hypertension and can be normalized by treatment with lisinopril. A depressed degradation of collagen type I may facilitate organ fibrosis in hypertensive patients, namely, in those with left ventricular hypertrophy.