Tricuspid valve orifice and tricuspid valve anulus areas were measured simultaneously in the anesthetized dog with a newly developed area-measuring system based on electromagnetic induction. This system permitted real-time monitoring of the area enclosed by the edges of valve leaflets and by the juncture of the valve leaflet and the cardiac wall in situ, without artificial constraint to the valve motion. Right atrial and right ventricular pressures were measured with two catheter-tipped micromanometers. During control state, tricuspid valve orifice area (TOA) increased up to its peak [1.38±0.26 cm2(mean±SD)] coincidently with either atrial systole or rapid ventricular filling. Atrial contraction evoked distinct presystolic tricuspid anulus narrowing with concomitant slow TOA reduction. This slow TOA reduction began 30.0±16.1 msec before systolic atrioventricular pressure crossover, and the following rapid TOA decrease was completed 38.7 ±12.2 msec after systolic atrioventricular pressure crossover. TOA began to increase 48.4±30.4 msec before diastolic atrioventricular pressure crossover at the end portion of the isovolumic relaxation phase, opposing residual transvalvular pressure gradient (3.33±1.79 mm Hg). The slow presystolic TOA decrease was considered to be a reflection of the presystolic anulus narrowing caused by atrial systole. An Isolated atrial contraction induced by administering 1 mg acetylcholine chloride into the atrioventricular node artery or by vagus nerve stimulation could produce complete valve closure. Even in an isolated atrial contraction, the inflection point that marks the boundary between slow "atriogenic" closure presumably due to anulus narrowing and rapid closure presumably due to hemodynamic force was easily identified.