Figure 1.

Typical recordings of the effects of nifedipine on the spontaneous electrical and Ca²⁺ signals in the mouse renal pelvis. (A) In some preparations, regenerative action potentials recorded in typical smooth muscle cells (TSMCs) (Aai) were completely blocked in 1 μM nifedipine (Aaii); dashed line represents 0 mV. In other preparations (Abi–ii), although the time course and amplitude of TSMC action potential were significantly reduced in 1 μM nifedipine; their frequency of discharge often increased. (Bi–ii) High frequency spontaneous transient depolarizations (STDs) were recorded in approximately 50% of impalements and either little affected or more evident (Abii) in 1 μM nifedipine. (Ci–ii) Long plateau action potentials, which did not trigger muscle contraction were occasionally recorded (at frequency of 1–3 min⁻¹) and little affected by 1 μM nifedipine. (Di–ii) Ca²⁺ waves in TSMC layer were either completely blocked or partially reduced (Di) in 1 μM nifedipine. Ca²⁺ transients were recorded in spindle-shaped ASMCs (E) and fusiform interstitial cells of Cajal-like cells (ICC-LCs) (F) distinguished by their distinctive discharge frequency and time course were little affected by 1 μM nifedipine. (G) Greyscale fluorescence micrographs of cells displaying Ca²⁺ transients in TSMC layer (Gi) in the absence of nifedipine and ASMCs (Gii) and ICC-LCs (Giii) in 1 μM nifedipine. Calibration bars represent 30 μm.