Penile tumescence and rigidity are considered to be a purely vascular process related to an increased inflow and a decreased outflow. This theory, which provides a satisfactory explanation for tumescence, is unable to explain the existence of high intracavernous pressures recorded both in animals and in man. Based on a hydrostatic model, the authors distinguish two phases involving different physiological mechanisms: an infrasystolic vascular phase and a suprasystolic muscular phase. During the vascular phase, the intracavernous pressure (ICP) can never exceed the systolic blood pressure. However, during the muscular phase, the ICP largely exceeds the systolic pressure, reaching values as high as 400 mmHg in man and 1,000 mmHg in animals. These variations in ICP can be explained by the contraction of perineal muscles, particularly the ischiocavernosus muscles. Various animal and human experiments are presented in support of this hypothesis. The pressure variations exerted on the glans during coitus by the perivaginal musculature are sufficient to induce reflex contractions of the ischiocavernosus muscles, promoting penile rigidity.