We investigated the origin of spontaneous transient inward current (STIC) oscillations in descending vasa recta (DVR) pericytes. In cells clamped at −80 mV, angiotensin II (ANG II; 10 nmol/l) induced oscillations with mean amplitude and frequency of −65.5 pA and 1.2 Hz. Simultaneous recording of cytoplasmic calcium ([Ca²⁺]_CYT) and membrane current oscillations verified their synchrony and the correlation of their amplitudes. Confocal recording in fluo-4-loaded DVR showed that ANG II can induce either stable pericyte [Ca²⁺]_CYT elevation or oscillations, while decreasing adjacent endothelial [Ca²⁺]_CYT. Oscillating currents reversed sign at −30.2 mV and were blocked by niflumic acid, implicating charge transfer via Cl⁻ ion. Removal of extracellular Ca²⁺, blockade of Ca²⁺ influx with SKF96365 (30 μmol/l), ryanodine (30 μmol/l), or caffeine (10 mmol/l) inhibited oscillations. In contrast, they were insensitive to removal of extracellular Na⁺ and exposure to either nifedipine (1 μmol/l) or 2-aminoethoxydiphenyl borate (10 μmol/l). Ouabain (100 nmol/l) increased basal pericyte [Ca²⁺]_CYT and the frequency of resting STICs but did not affect the larger oscillations that followed ANG II stimulation. We conclude that [Ca²⁺]_CYT oscillations stimulate Cl⁻ currents. The former are most likely maintained by repetitive cycles of ryanodine-sensitive SR Ca²⁺ release and SKF96365-sensitive store refilling.