Depolarisation of cardiac cells causes calcium (Ca2+) release from an intracellular store known as the sarcoplasmic reticulum (SR). The transient elevation in intracellular Ca2+ concentration that results causes cardiac contraction. SERCA2a enables cardiac relaxation when it pumps Ca2+ back into the SR hence refilling the Ca2+ store for the next contraction. The abundances of SERCA2a differ in atria and ventricles of various species so that relaxation times are shorter in atria under normal conditions (Freestone et al., 1999). We show that SERCA2a has a tendency to be differently expressed in different chambers from healthy and diseased rat hearts. Left and right atria and ventricles from rats experimentally-induced to manifest heart failure (aorto-caval shunt causing volume overload) and sham-operated Wistar rats, as well as spontaneously hypertensive rats (SHR) and their normotensive controls were snap frozen and homogenised. Western blotting was carried out and the protein abundance was quantitatively determined by densitometry. Sham-operated and normotensive animals had a tendency to have a higher abundance of SERCA2a than animals with heart failure and hypertension in both atrial and ventricular tissues as shown in Table 1. The ventricular tissue expresses less SERCA2a compared to the atria in both normal and hypertensive animal populations. A trend arises where there is a tendency for less SERCA2a protein in the disease state compared to the normal state. SERCA2a has a tendency to be less expressed in heart failure tissues (especially for left ventricular and left atrial shunt and sham-operated tissues, p = 0.1). SERCA2a also has a tendency to be expressed more in WKY compared to SHR for all four heart chambers, which may relate to less Ca2+ release in the SHR animals and consequently less forceful contractions of the hypertrophied heart (Li et al., 2005). SERCA2a is therefore expressed in a chamber-specific manner in the cardiac tissue samples of both healthy and diseased heart.