End diastolic volume is the primary determinant of preload. Frank Starling mechanism explains how an increased preload leads to an increased stroke volume.
It states that ventricular muscle fibers stretching which happens with increasing end diastolic volume causes greater overlap between myosin and actin within sarcomeres.
This will lead to greater velocity and extent of shortening of myocyte during contraction.
As a results it leads to a stronger ventricular contraction and larger stroke volume.
This allows ejection fraction of the heart to be maintained in the face of increase preload.
Another theory indicates that cardiac troponin becomes increasingly sensitive to cytosolic calcium at greater lengths of sarcomere.
This results in increased calcium binding which leads to an increase in force of muscle contraction.
Venodilators / diuretics able to reduce preload by decreasing the intravascular volume. Therefore it can be used to lower the blood pressure.
However, in the case of heart failure, increasing preload may lead to less efficient ventricular contraction and a smaller stroke volume.