Calcium-antagonism: A new therapeutic access to hypertensive heart disease

  • Wolfgang Motz
  • B. E. Strauer
Conference paper


We studied in spontaneously hypertensive rats (SHR) whether a chronic antihypertensive treatment with the calcium antagonist nifedipine can prevent later deterioration in left ventricular (LV) function as frequently seen in sustained arterial hypertension. After treatment (60 weeks) with nifedipine (30 mg/kg body weight and day), LV pumping function was considerably augmented (cardiac index: + 25.7 %; LV ejection fraction: + 13 %) due to a marked systolic unloading of the left ventricle (systolic wall stress: −22.9 %) in comparison to untreated animals. Myocardial isometric function, which was assessed by the maximum actively developed LV systolic wall stress when totally occluding the proximal aorta, remained preserved in the nifedipine group whereas it decreased by 10.9 % in the untreated subjects. We conclude that in SHR later LV dysfunction can be prevented by an early onset of antihypertensive treatment with nifedipine.

Key words

nifedipine left ventricular function myocardial contractility left ventricular afterload left ventricular hypertrophy left ventricular systolic wall stress left ventricular systolic wall stress reserve 


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  1. 1.
    Guazzi, M. D., C. Fiorentini, M. T. Olivari, T. Bartorelli, G. Neechi, A. Polese: Short-and long-term efficiency of a calcium-antagonistic agent (nifedipine) combined with methyldopa in the treatment of severe hypertension. Circulation 61, 913–919 (1980).PubMedGoogle Scholar
  2. 2.
    Motz W., M. Ploeger, G. Ringsgwandl, N. Goeldel, B. Garthoff, S. Kazda, B. E. Strauer: The influence of nifedipine on ventricular function and myocardial hypertrophy in spontaneously hypertensive rats. J. Cardiovasc. Pharmacol. 5, 55–61 (1983).PubMedCrossRefGoogle Scholar
  3. 3.
    Meerson, F. S.: Hyperfunktion, Hypertrophie und Insuffizienz des Herzens, VEB Volk nd Gesundheit (Berlin 1969).Google Scholar
  4. 4.
    Alpert, N.: Cardiac hypertrophy Academic press (New York 1971).Google Scholar
  5. 5.
    Strauer, B. E.: Myocardial oxygen consumption in chronic heart disease. Role of wall stress, hypertrophy and coronary reserve. Amer. J. Cardiol. 44, 730 (1979).Google Scholar
  6. 6.
    Sachs, L.: Angewandte Statistik. Springer (Berlin-Heidelberg-New York 1974).Google Scholar
  7. 7.
    Fleckenstein-Grün, A. Fleckenstein: Calcium-Antagonismus, ein Grundprinzip der Vasodilatation. In: Calcium-Antagonismus, edited by Fleckenstein, A., H., Roskamm, p. 191 Springer (Berlin-Heidelberg-New York 1980).CrossRefGoogle Scholar
  8. 8.
    Strauer, B. E.: Hypertensive Heart Disease. Springer (Berlin-Heidelberg-New York 1980).CrossRefGoogle Scholar
  9. 9.
    Bürger, S., B. E. Strauer: Left ventricular hypertrophy in chronic pressure load due to essential hypertension. I. Left ventricular function, left ventricular geometry and wall stress. In: The Heart in Hypertension, edited by B. E. Strauer, p. 13 Springer (Berlin-Heidelberg-New York 1981).Google Scholar
  10. 10.
    Ludbrook, P. A., A. J. Tiefenbrunn, B. E. Sobel: Influence of nifedipine on left ventricular systolic and diastolic function. Relationship to manifestions of ischemia and congestive heart failure. Amer. J. Med. 71, 683 (1981).Google Scholar
  11. 11.
    Motz, W., B. E. Strauer: The influence of nifedipine on left ventricular compliance and myocardial stiffness. J. Amer. College Cardiol. (1983) in press.Google Scholar
  12. 12.
    Kaltenbach, M., W. Schulz, T. Kober: Effects of nifedipine after intravenous and intracoronary administration. Amer. J. Cardiol. 44, 832 (1979).PubMedCrossRefGoogle Scholar

Copyright information

© Dr. Dietrich Steinkopff Verlag, GmbH & Co. KG, Darmstadt 1983

Authors and Affiliations

  • Wolfgang Motz
    • 1
  • B. E. Strauer
    • 1
  1. 1.Medizinische Klinik IUniversität München, Klinikum GroßhadernMünchen 70Germany

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