1.Angiotensin levels are increased in Hypertension. It is increased by intake of corticosteroids (they upregulate angiotensin II synthesis), estrogen, thyroid hormones and angiotensin which stimulate the renin-angiotensin which increases the blood pressure by causing vasoconstriction which leads to hypertension.

2.ACE inhibitors not only block the conversion of ANG I to ANG II but also inhibit the degradation of bradykinin which causes vasodilation implying that there will be a decrease in blood pressure leading to hypotension. Inhibition of the metabolism of Bradykinin increases vascular permeability causing angioedema and a cough. Whereas the drugs that block the angiotensin receptors are specific competitive antagonists and have a lower incidence of a cough.

3.ACE inhibitors inhibit the d=metabolism of bradykinin which has vasodilatory effects, therefore it decreases the blood pressure. They also decrease peripheral ventricular resistance which decreases the blood pressure.

4. Losartan blocks angiotensin AT1 receptor only. Prolonged treatment with the use of Losartan causes may cause stimulation of angiotensin AT2 receptors

5. Kinins causes vasodilation on the arteries and vasoconstriction on the veins. The vasodilation may result from a direct inhibitory effect of kinins on arteriolar smooth muscle or may be mediated by the release of nitric oxide or vasodilator prostaglandins such as PGE2 and PGI2. Vasoconstriction may result from direct stimulation of venous smooth muscle or from the release of venoconstrictor prostaglandins such as PGF2α. Prostaglandin is a potent vasodilator.

6. The receptors involved in the clinical effects of kinins are the beta receptors.

7. Natriuretic peptides produce vasodilation which will decrease your blood pressure therefore brin helpful in the treatment of hypertension and congestive heart failure. increase in ANP and BNP causes natriuresis and vasodilation, as well as a compensatory increase in renin secretion and plasma ANG II levels. The development of drugs that combine neprilysine inhibition with an ACE inhibitor in order to prevent the increase in plasma ANG II, or with an ARB to block the actions of ANG II.

8. Neprilysin is a neutral endopeptidase and it is inhibited to prevent an increase in plasma ANG II  which increases hypertensive effects and heart failure and an example is Sacubitril (valsartan).

9. vasodilators: PGI2 and Nitric Oxide

vasoconstrictors: Endothelin ET1, ET2, ET3