Dihydropyridines such as BAY K8644 and the benzoylpyrole derivative FPL 64176 are pharmacological agents well known for their agonist action to activate L-type VGCCs. Studies exploring the modulation of GPCR mobilization of intracellular calcium often involve the use of agonists and antagonists of L-type voltage-gated calcium channels (L-type VGCCs) to distinguish between increases in intracellular calcium due to extracellular influx from those associated with intracellular calcium release due to activation of inositol triphosphate receptors (IP3R) on intracellular calcium stores. However, direct interference on calcium mobilisation due to L-type calcium channels drugs is an unreported observation; one which could confound interpretation of calcium measurement data. White fat adipocytes (WFA) were isolated from epididymal fat of CD-1 mice by standard methods. Intracellular calcium ([Ca2+]i) measurements were made by epifluorescent microscopy at 28°C. We found that the L-type VGCC agonists 10 µM Bay K 8644 (n=15) and 1 µM FPL 64176 (n=20) abolished the mobilisation of intracellular calcium in WFA evoked by 100 nM oxytocin (p<0.05, Kruskall Wallis). In contrast, 20 nM growth hormone which biochemically upregulates L-type VGCCs in these cells was without effect on the oxytocin response. The inhibition of intracellular calcium mobilisation by BAY K8644 and FPL 64174 was neither time-dependent, nor vehicle-mediated; as oxytocin was able to elicit a characteristic transient increase in intracellular calcium after a prolonged period of 25 minutes (n=20) in the absence of both agents. In addition, dimethyl sulfoxide (n=18), the vehicle for both L-type VGCC agonists had no inhibitory effect on oxytocin action. Our data suggest that the actual drug themselves: BAY K8644 and FPL 64174 directly interfere with calcium mobilisation by oxytocin, and not by an increase in  L-type calcium channel activity per se. Whether this effect is unique to WFA or/and oxytocin remains to be investigated.