Cardiovascular end-organ damage in Ren-2 transgenic rats compared to spontaneously hypertensive rats

Y. M. Pinto; H. Buikema; W. H. van Gilst; E. Scholtens; P. P. van Geel; P. A. de Graeff; J. Wagner; M. Paul

doi:https://doi.org/10.1007/s001090050123

Cardiovascular end-organ damage in Ren-2 transgenic rats compared to spontaneously hypertensive rats

Y. M. Pinto, H. Buikema, W. H. van Gilst, E. Scholtens, P. P. van Geel, P. A. de Graeff, J. Wagner, M. Paul

Other Departments

Research output: Contribution to journal › Article › Academic › peer-review

45 Citations (Scopus)

Abstract

To compare hypertensive end-organ damage in two genetic forms of hypertension we assessed cardiovascular function in two rat strains of genetic hypertension: transgenic rats overexpressing the mouse Ren-2 gene [(TGR(mREN2)27]) and blood pressure matched spontaneously hypertensive rats (SHR). Despite similarly elevated blood pressure, systolic dp/dt (mmHg/s) was more impaired in transgenic rats (3099 +/- 446) than in SHR (3571 +/- 272) and normals (4342 +/- 119; P <0.05). Left ventricular weight (mg/g body weight) increased more in the transgenic rats (40 +/- 3) than in SHR (31 +/- 2) and normals (26 +/- 2). Endothelium-dependent relaxation was significantly decreased only in the transgenic rats. This study shows significantly more cardiac and endothelial dysfunction in transgenic, hypertensive TGR (mREN2)27 than in age and blood pressure matched SHR. This supports the hypothesis that chronic activation of the renin-angiotensin system significantly contributes to hypertensive end-organ damage

Original language	English
Pages (from-to)	371-377
Journal	Journal of molecular medicine (Berlin, Germany)
Volume	75
Issue number	5
DOIs	https://doi.org/10.1007/s001090050123
Publication status	Published - 1997

Access to Document

https://doi.org/10.1007/s001090050123

Cite this

@article{c4606c0b9ac4473695ad94ccd09cc29f,

title = "Cardiovascular end-organ damage in Ren-2 transgenic rats compared to spontaneously hypertensive rats",

abstract = "To compare hypertensive end-organ damage in two genetic forms of hypertension we assessed cardiovascular function in two rat strains of genetic hypertension: transgenic rats overexpressing the mouse Ren-2 gene [(TGR(mREN2)27]) and blood pressure matched spontaneously hypertensive rats (SHR). Despite similarly elevated blood pressure, systolic dp/dt (mmHg/s) was more impaired in transgenic rats (3099 +/- 446) than in SHR (3571 +/- 272) and normals (4342 +/- 119; P <0.05). Left ventricular weight (mg/g body weight) increased more in the transgenic rats (40 +/- 3) than in SHR (31 +/- 2) and normals (26 +/- 2). Endothelium-dependent relaxation was significantly decreased only in the transgenic rats. This study shows significantly more cardiac and endothelial dysfunction in transgenic, hypertensive TGR (mREN2)27 than in age and blood pressure matched SHR. This supports the hypothesis that chronic activation of the renin-angiotensin system significantly contributes to hypertensive end-organ damage",

author = "Pinto, {Y. M.} and H. Buikema and {van Gilst}, {W. H.} and E. Scholtens and {van Geel}, {P. P.} and {de Graeff}, {P. A.} and J. Wagner and M. Paul",

year = "1997",

doi = "https://doi.org/10.1007/s001090050123",

language = "English",

volume = "75",

pages = "371--377",

journal = "Journal of molecular medicine (Berlin, Germany)",

issn = "0946-2716",

publisher = "Springer Verlag",

number = "5",

}

TY - JOUR

T1 - Cardiovascular end-organ damage in Ren-2 transgenic rats compared to spontaneously hypertensive rats

AU - Pinto, Y. M.

AU - Buikema, H.

AU - van Gilst, W. H.

AU - Scholtens, E.

AU - van Geel, P. P.

AU - de Graeff, P. A.

AU - Wagner, J.

AU - Paul, M.

PY - 1997

Y1 - 1997

N2 - To compare hypertensive end-organ damage in two genetic forms of hypertension we assessed cardiovascular function in two rat strains of genetic hypertension: transgenic rats overexpressing the mouse Ren-2 gene [(TGR(mREN2)27]) and blood pressure matched spontaneously hypertensive rats (SHR). Despite similarly elevated blood pressure, systolic dp/dt (mmHg/s) was more impaired in transgenic rats (3099 +/- 446) than in SHR (3571 +/- 272) and normals (4342 +/- 119; P <0.05). Left ventricular weight (mg/g body weight) increased more in the transgenic rats (40 +/- 3) than in SHR (31 +/- 2) and normals (26 +/- 2). Endothelium-dependent relaxation was significantly decreased only in the transgenic rats. This study shows significantly more cardiac and endothelial dysfunction in transgenic, hypertensive TGR (mREN2)27 than in age and blood pressure matched SHR. This supports the hypothesis that chronic activation of the renin-angiotensin system significantly contributes to hypertensive end-organ damage

AB - To compare hypertensive end-organ damage in two genetic forms of hypertension we assessed cardiovascular function in two rat strains of genetic hypertension: transgenic rats overexpressing the mouse Ren-2 gene [(TGR(mREN2)27]) and blood pressure matched spontaneously hypertensive rats (SHR). Despite similarly elevated blood pressure, systolic dp/dt (mmHg/s) was more impaired in transgenic rats (3099 +/- 446) than in SHR (3571 +/- 272) and normals (4342 +/- 119; P <0.05). Left ventricular weight (mg/g body weight) increased more in the transgenic rats (40 +/- 3) than in SHR (31 +/- 2) and normals (26 +/- 2). Endothelium-dependent relaxation was significantly decreased only in the transgenic rats. This study shows significantly more cardiac and endothelial dysfunction in transgenic, hypertensive TGR (mREN2)27 than in age and blood pressure matched SHR. This supports the hypothesis that chronic activation of the renin-angiotensin system significantly contributes to hypertensive end-organ damage

U2 - https://doi.org/10.1007/s001090050123

DO - https://doi.org/10.1007/s001090050123

M3 - Article

C2 - 9181479

SN - 0946-2716

VL - 75

SP - 371

EP - 377

JO - Journal of molecular medicine (Berlin, Germany)

JF - Journal of molecular medicine (Berlin, Germany)

IS - 5

ER -