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Related Experiment Videos

Senescent heart compared with pressure overload-induced hypertrophy

P Assayag1, D Charlemagne, J de Leiris

  • 1Institut National de la Santé et de la Recherche Médicale (INSERM) U127, IFR Circulation, Hôpital Lariboisière, Paris, France.

Hypertension (Dallas, Tex. : 1979)
|January 1, 1997
PubMed
Summary

Aging impairs heart contractility through reduced SERCA2 mRNA, despite normal systolic function in elderly rats. Compensatory mechanisms maintain in vivo function, but hypertension is fatal in aged rats.

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Area of Science:

  • Cardiology
  • Gerontology
  • Molecular Biology

Background:

  • Aging is associated with cardiac alterations, including sarcoplasmic reticulum Ca2+ ATPase changes, even with normal systolic function in the elderly.
  • Alterations in other calcium-regulating proteins in aging hearts are not well understood.

Purpose of the Study:

  • To investigate age-related changes in left ventricular (LV) function and calcium-regulating proteins (Na(+)-Ca2+ exchanger (NCx), ryanodine receptor (RyR2), and sarcoplasmic reticular Ca2+ ATPase (SERCA2)).
  • To compare the effects of renovascular hypertension on hemodynamics and calcium proteins in adult and aged rats.

Main Methods:

  • Measured hemodynamics and mRNA levels of NCx, RyR2, and SERCA2 in adult and senescent rat left ventricles.
  • Assessed ex vivo contractile function (active tension) during isolated heart perfusion.

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  • Induced renovascular hypertension or sham operation in adult and aged rats.

    • Main Results:

    • Senescent rats showed depressed active tension but unaltered LV systolic pressure and maximal rates of pressure development.
    • SERCA2 mRNA levels were decreased in senescent rat left ventricles, while NCx and RyR2 mRNA levels remained unchanged.
    • Renovascular hypertension caused 100% mortality in aged rats and induced LV hypertrophy and decreased SERCA2 mRNA in adult rats.

    Conclusions:

    • Contractile dysfunction in senescent hearts is linked to decreased SERCA2 mRNA, with compensatory mechanisms preserving in vivo function.
    • RyR2 and NCx gene expressions are not implicated in the observed age-related contractile dysfunction.
    • Aged rats are highly susceptible to renovascular hypertension, unlike adult rats, suggesting age-dependent vulnerability.