Renin promoter SV40 T-antigen transgenic mouse. A model of primary renal vascular hyperplasia. Hypertension 1991 Jun;17(6 Pt 2):1167-62
Date
06/01/1991Pubmed ID
2045162DOI
10.1161/01.hyp.17.6.1167Scopus ID
2-s2.0-0026095260 (requires institutional sign-in at Scopus site) 16 CitationsAbstract
Transgenic mice containing a ren-2 promoter T-antigen fusion construct (TAG+) develop renal vascular hypertrophy and hyperplasia associated with markedly suppressed renal renin mRNA, renal renin content, and plasma renin concentration. These animals are normotensive. In the present study, the renal and cardiovascular systems are characterized, revealing some surprising findings. Not only are the TAG+ mice normotensive in the face of pronounced renal pathology but also in the presence of an increase in plasma volume. These data raise interesting questions about blood pressure physiology and renal function of the TAG+ mice. Blood nitrogen urea of the TAG+ animal was markedly elevated and plasma creatinine level was in the normal range, indicating prerenal azotemia without renal failure. These findings are consistent with impaired renal perfusion with secondary volume expansion probably as the result of vascular hyperplasia. These transgenic animals provide a unique genetic model for studying the physiology of primarily renal vascular hyperplasia as well as blood pressure control in a low renin state.
Author List
Jacob HJ, Sigmund CD, Shockley TR, Gross KW, Dzau VJAuthor
Curt Sigmund PhD Chair, Professor in the Physiology department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsAntigens, Polyomavirus Transforming
Blood Pressure
Blood Vessels
Blood Volume
Hematocrit
Hyperplasia
Kidney
Mice
Mice, Transgenic
Promoter Regions, Genetic
Renal Circulation
Renin
