Objective. Spliced isoforms of the voltage-gated calcium channel (VGCC) gene CACN1C are differentially expressed along the vascular tree. These isoforms display cell-specific electrophysiological properties with respect to the window VGCC Ca²⁺ influx and sensitivity to L-type Ca²⁺ channel blockers. We investigated whether the window VGCC Ca²⁺ influx plays a physiological role for blood vessel constriction. Methods. Ca²⁺ mobilisation (Fura-2 assay) and isometric contraction were studied in aortic segments of C57Bl6 mice. The membrane potential was clamped at fixed potentials by increasing external K⁺ concentration. Results. Above 20 mM, K⁺ induced biphasic contractions. The fast component coincided with Ca²⁺ influx via a VGCC population that exhibited fast activation and then inactivation. The slow force component was temporally related to a slow voltage-dependent, but time-independent Ca²⁺ influx, which was not due to Ca²⁺ induced Ca²⁺ release, as it was not affected by dantrolene, ryanodine or cyclopiazonic acid. By modulating external Ca²⁺ levels before and after depolarisation with extracellular K⁺, we could attribute the sustained contraction to a population of VGCCs displaying incomplete inactivation (window). At normal extracellular K⁺ concentration, this window was operative, allowing a continuous VGCC-mediated Ca²⁺ influx leading to basal tone. Basal influx and force were both suppressed upon hyperpolarization by adding the ATP-dependent K⁺ channel agonist levcromakalim and enhanced by adding the VGCC agonist BAY K8644. Conclusion. Basal tension and isometric contraction of C57Bl6 mouse aortic smooth muscle cells are mediated by voltage-dependent window L-type Ca²⁺ influx.