gms | German Medical Science

27. Wissenschaftlicher Kongress der Deutschen Hochdruckliga

Deutsche Liga zur Bekämpfung des hohen Blutdrucks – Deutsche Hypertonie Gesellschaft e. V.

26. bis 29.11.2003, Bonn

Genetic deficit of nephron number aggravates left ventricular hypertrophy and dysfunction in hypertension due to renal mass reduction

Angeborener Nephron-Mangel verstärkt linksventrikuläre Hypertrophie und Dysfunktion nach Nierenteilresektion

Meeting Abstract (Hypertonie 2003)

  • presenting/speaker M. Lorenz - Berlin, D
  • A. Schnieber - Berlin, D
  • I. Bauhaus - Berlin, D
  • J. Eberson - Berlin, D
  • M. Wehland - Berlin, D
  • M. Paul - Berlin, D
  • W. Zidek - Berlin, D
  • R. Kreutz - Berlin, D
  • L. Rothermund - Berlin, D

Hypertonie 2003. 27. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Bonn, 26.-29.11.2003. Düsseldorf, Köln: German Medical Science; 2004. Doc03hochP64

The electronic version of this article is the complete one and can be found online at:

Published: November 11, 2004

© 2004 Lorenz et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.




Inborn nephron number is an important factor for manifestation of primary hypertension. This study investigated the relevance of genetic nephron number deficit for development of left ventricular hypertrophy (LVH) and left ventricular (LV) dysfunction in hypertension due to renal mass reduction.

Methods and Results

Munich Wistar Fömter (MWF) rats with a genetic reduction of nephron number were compared to Wistar rats with normal nephron number. At 8 weeks of age animals underwent sham-operation (sham), renal mass reduction (Nx), or Nx and treatment with the angiotensin-converting enzyme inhibitor ramipril (ACE) for 4 weeks.

Systolic blood pressure (SBP), LV weight, LV enddiastolic pressure (LVEDP), LV mRNA expression of atrial natriuretic factor (ANF) were elevated, and +dP/dtmax and -dP/dtmax were decreased in both MWF-Nx and Wistar-Nx groups compared to their sham-operated controls (p<0.05, respectively). Dependent on nephron number, SBP, LV weight, LVEDP were increased, and +dP/dtmax and -dP/dtmax were reduced in MWF-Nx compared to Wistar-Nx (p<0.05, respectively). Treatment with ramipril in MWF-Nx-ACE and Wistar-Nx-ACE did lower SBP, LV weight, completely prevented the deterioration of LVEDP, LV ANF mRNA expression, +dP/dtmax and -dP/dtmax compared to MWF-Nx (p<0.05, respectively).


Genetic deficit in nephron number aggravates LVH and LV dysfunction that develops in hypertension due to renal mass reduction. ACE inhibition exerts its cardiovascular protection independent of inborn nephron number.