Structural and functional alterations in the Ca$^2+$ regulatory
proteins present in the sarcoplasmic reticulum have recently been
shown to be strongly involved in the pathogenesis of heart failure.
Chronic activation of the sympathetic nervous system or of the renin-angiotensin
system induces abnormalities in both the function and structure of
these proteins. We review here the considerable body of evidence
that has accumulated to support the notion that such abnormalities
contribute to a defectiveness of contractile performance and hence
to the progression of heart failure.