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Dynamic changes in sarcoplasmic reticulum function in cardiac hypertrophy and failure.

G Szymanska¹, H Strömer, D H Kim

¹Boston College, MA 02167, USA.

Pflugers Archiv : European Journal of Physiology

|January 29, 2000

Summary

Pressure overload impairs cardiac relaxation by altering sarcoplasmic reticulum (SR) function. Reduced SR Ca2+ uptake and release contribute to impaired relaxation in hypertrophied and failing hearts.

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Area of Science:

Cardiology
Molecular Biology
Physiology

Background:

Cardiac function is altered by pressure overload-induced hypertrophy.
Sarcoplasmic reticulum (SR) plays a crucial role in cardiac muscle contraction and relaxation by regulating intracellular calcium (Ca2+).

Purpose of the Study:

To investigate the changes in sarcoplasmic reticulum (SR) Ca2+ uptake and release functions in pressure overload-induced cardiac hypertrophy and failure.
To correlate these SR function changes with impaired cardiac relaxation.

Main Methods:

Isolated, perfused hypertrophied rat hearts subjected to ascending aorta banding.
Measurement of SR Ca2+ uptake rates and maximum transport rate (Vmax) using oxalate-supported assays.
Assessment of SR Ca2+ pump affinity for Ca2+ (EC50) and SR Ca2+ release channel activity via [3H] ryanodine binding (Bmax).

Keywords:

Non-programmatic

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Main Results:

Prolonged cardiac relaxation time was observed in compensated hypertrophy and failure.
Reduced SR Ca2+ pump affinity (increased EC50) and decreased SR Ca2+ pump amount (decreased Vmax) were found with progressive hypertrophy.
A significant reduction in SR Ca2+ release channels (decreased Bmax) was noted in hypertrophied and failing hearts.

Conclusions:

Pressure overload leads to impaired cardiac relaxation due to diminished SR Ca2+ uptake and release.
These alterations in SR Ca2+ handling contribute to the progression of cardiac hypertrophy and failure.