—To investigate the cellular mechanisms for altered Ca²⁺ homeostasis and contractility in cardiac hypertrophy, we measured whole-cell L-type Ca²⁺ currents (I_Ca,L), whole-cell Ca²⁺ transients ([Ca²⁺]_i), and Ca²⁺ sparks in ventricular cells from 6-month-old spontaneously hypertensive rats (SHRs) and from age- and sex-matched Wistar-Kyoto and Sprague-Dawley control rats. By echocardiography, SHR hearts had cardiac hypertrophy and enhanced contractility (increased fractional shortening) and no signs of heart failure. SHR cells had a voltage-dependent increase in peak [Ca²⁺]_i amplitude (at 0 mV, 1330±62 nmol/L [SHRs] versus 836±48 nmol/L [controls], P<0.05) that was not associated with changes in I_Ca,L density or kinetics, resting [Ca²⁺]_i, or Ca²⁺ content of the sarcoplasmic reticulum (SR). SHR cells had increased time of relaxation. Ca²⁺ sparks from SHR cells had larger average amplitudes (173±192 nmol/L [SHRs] versus 109±64 nmol/L [control]; P<0.05), which was due to redistribution of Ca²⁺ sparks to a larger amplitude population. This change in Ca²⁺ spark amplitude distribution was not associated with any change in the density of ryanodine receptors, calsequestrin, junctin, triadin 1, Ca²⁺-ATPase, or phospholamban. Therefore, SHRs with cardiac hypertrophy have increased contractility, [Ca²⁺]_i amplitude, time to relaxation, and average Ca²⁺ spark amplitude (“big sparks”). Importantly, big sparks occurred without alteration in the trigger for SR Ca²⁺ release (I_Ca,L), SR Ca²⁺ content, or the expression of several SR Ca²⁺-cycling proteins. Thus, cardiac hypertrophy in SHRs is linked with an alteration in the coupling of Ca²⁺ entry through L-type Ca²⁺ channels and the release of Ca²⁺ from the SR, leading to big sparks and enhanced contractility. Alterations in the microdomain between L-type Ca²⁺ channels and SR Ca²⁺ release channels may underlie the changes in Ca²⁺ homeostasis observed in cardiac hypertrophy. Modulation of SR Ca²⁺ release may provide a new therapeutic strategy for cardiac hypertrophy and for its progression to heart failure and sudden death.