During the cardiac action potential, Ca²⁺ entry through dyhidropyridine receptor L-type Ca²⁺ channels (DHPR) activates ryanodine receptor (RyR) Ca²⁺ release channels, resulting in massive Ca²⁺ mobilization from the sarcoplasmic reticulum (SR). This global Ca²⁺ release arises from spatio-temporal summation of many localized elementary Ca²⁺ release events, Ca²⁺ sparks. We tested whether DHPRs modulate Ca²⁺ sparks in a Ca²⁺ entry-independent manner. Negative modulation by DHPR of RyRs via physical interactions is accepted in resting skeletal muscle but remains controversial in heart. Ca²⁺ sparks were studied in cat cardiac myocytes permeabilized with saponin or internally perfused via a patch pipette. Bathing and pipette solutions contained low Ca²⁺ (100 nM). Under these conditions, Ca²⁺ sparks were detected with a stable frequency of 3-5 sparks·s^-1·(100 µm)^-1. The DHPR blockers nifedipine, nimodipine, FS-2 and calciseptine decreased spark frequency while DHPR agonists Bay-K8644 and FPL-64176 increased it. None of these agents altered the spatio-temporal characteristics of Ca²⁺ sparks. The DHPR modulators were also without effect on SR Ca²⁺ load (caffeine-induced Ca²⁺ transients) or SR Ca²⁺-ATPase (SERCA) activity (Ca²⁺ loading rates of isolated SR microsomes) and did not change cardiac RyR channel gating (planar lipid bilayer studies). In summary, DHPR modulators affected spark frequency in the absence of DHPR-mediated Ca²⁺ entry. This action could not be attributed to a direct action of DHPR modulators on SERCA or RyR. Our results suggest that the activity of RyR Ca²⁺ release units in ventricular myocytes is modulated by Ca²⁺ entry-independent conformational changes in neighboring DHPRs.