1.    Hypertension: Increased angiotensinogen levels increases angiotensin leading to increased blood pressure.
Oedema: increased angiotensinogen levels increases water retention leading to increased blood pressure.
2.    ACE is also involved in bradykinin metabolism which will decrease prostaglandin synthesis and increases vasoconstriction. Angiotensin receptor blockers are selective causing less side effects.
3.    Angiotensin 1 is not converted to angiotensin 2 by ACE, preventing the cascade leading to increased blood pressure. ACE inhibitors prevent inactivation of bradykinin leading to increased prostaglandin synthesis, vasodilation and decreased blood pressure. 
4.    Losartan and other similar drugs are selective AT1 receptor blockers and will have a direct effect on AT1 receptors by decreasing angiotensin 2.
5.    Kinins are vasodilatory peptides and they increase capillary permeability. Other autocoids which are vasodilatory include natriuretic peptides, CGRP, vasoactive intestinal peptides, substance P, neurokinin A and B.
6.    G-protein coupled receptors.
7.    They are vasodilatory, therefore they are used to decrease blood pressure by vasodilation and renin excretion. Atrial natriuretic peptide plays a role in congestive heart failure and intravenous netritide (Brain natriuretic peptide) is used in severe heart failure.  
8.    Sacubitril inhibits neprilysin, which is a neutral endopeptidase responsible natriuretic peptide metabolism in the liver and kidneys. Natriuretic peptides are useful in heart failure. Sacubitril is also used in bleeding disorders and post-myocardial infarction by controlling blood volume.
9.    Bosentan is an ETA antagonist leading to vasodilation.
Nitric oxide and PG12 also cause vasodilation but their action is followed by prolonged vasoconstriction.