Preload is a load / degree of tension on the ventricular muscle when it started to contract.
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. 

Contractility is a measure of the form of contraction of ventricle at a given preload. 
A greater and forceful contraction will eject more fraction of blood from ventricle and this will increase the stroke volume. 
Sympathetic nervous system (beta1 adrenergic receptors) and para sympathetic nervous system (muscarinic M2 cholinergic receptors) on the ventricular myocytes regulate the contractility of the ventricle.Beta blockers act by antagonising the sympathetic input into the myocardium. 
Based on the action, it will reduce contraction and leads to anti hypertensive effects. Stroke volume, oxygen demand and cardiac output will be reduced too. 
Contractility also increased by increasing the contraction of intracellular calcium. This can be achieved by the action of digitalis which decreased the extracellular calcium 
Contractility can also decrease by systolic dysfunction, hypercapnia, hypoxia, acidosis and calcium channel blockade. 

There are 3 main factors  affecting stroke volume which are preload, contractility and afterload. 

Cardiac output is the amount of blood which is pumped per unit time by the ventricles
Cardiac output is determined by the stroke volume which is the volume of blood ejected during each contraction of the ventricle and the frequency of heart beats ( heart rates)
The mathematical equation is : 
cardiac output = heart rate x stroke volume 
heart rate is under the control of autonomous nervous system.Beta blockers able to reduce the cardiac output by decreasing contractility and heart rate. 
Verapamil / diltiazem which is cardioselective (non-dihydropyridine) calcium channel blocker also able to reduce heart rate by slowing the transmission of impulse through the AV nodes.

Cardiology - Mean Arterial Pressure 
How to determine mean arterial pressure ? 
Mean arterial pressure is identified by considering how much blood the heart pumps into the arterial system at a given time ( cardiac output) and how much resistance that the arteries have to the flow of the blood ( total peripheral resistance). 
Mean arterial pressure ( MAP ) = Cardiac output (CA) x Total Peripheral Resistance ( TPR) 
Mean arterial pressure can also be calculated by using the following mathematical equation 
MAP = 1/3 systolic blood pressure + 2/3 diastolic blood pressure 
Cardiac output is the primary determinant of systolic blood pressure.
Total peripheral resistance is the primary determinant of diastolic blood pressure
1/3rd of cardiac cycle is in the systolic phase and 2/3 of the cardiac cycle is in the diastolic phase.