Article
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
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Published: | November 11, 2004 |
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Outline
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Background
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).
Conclusion
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.