Mean Arterial Pressure (MAP) = Cardiac Output (CO) x Total Peripheral Resistance (TPR)
Mean Arterial Pressure (MAP) = 1/3 x (Systolic Blood Pressure – Diastolic Blood Pressure)
CO = Stroke Volume (SV) x Heart Rate (HR)
Your MAP is monitored using your baroreceptors, found in the carotid sinus and the aortic arch. These are sensitive to changes in the blood pressures.

Changes in CO and TPR will causes changes to your MAP. For instance, TPR is affected by the radius of the blood vessels and the blood viscosity. CO is affected by by anything that affects your stroke volume (preload, contractility, afterload) as well as your heart rate.

Vasoconstrictors: Angiontensin-II, Catecholamines, Endothelin
Vasodilators: Prostaglandins , Nitric Oxide

However, in order to understand some basics concepts of blood pressure, you would need to revise the RAAS system. In a summary, Renin is released from the renal juxtaglomerual cells of the afferent arterioles. Renin is released in response to a decreased blood pressure, decreased sodium content of distal convoluted tubule, and increased catecholamines. Angiotensinogen, produced in the liver, is now released in the bloodstream. Renin converts Angiotensinogen into Angiotensin-I. Angiotensin-I is then converted in the lungs by the Angiotensin-Converting-Enzyme (ACE) into Angiotensin-II (a potent vasoconstrictor). Angiotensin-II has several effects, such as: Vasoconstriction, promotes Aldosterone (released by the Adrenal glands) secretion (increases Sodium and water reabsorption, increases potassium excretion), Sodium reabsorption, and increased thirst.

When there is too much intravascular volume, the myocardial natriuretic peptides (atrial (ANP) and B-type (BNP)) are released in response to dilatation of the chambers of the heart. These molecules result in inhibition of Sodium reabsorption, hence results in diuresis as well as results in vasodilation.