1.) Production of angiotensinogen is increased by corticosteriods, estrogens, thyroid hormones and ANG II. Elevated during pregnancy and in women taking estrogen containing contraceptives. Decreased blood pressure leads to more conversion of angiotensinogen to angiotensin II mediated by renin enzymes. This will thus increase the synthesis of angiotensinogen.

Implications include increased plasma angiotensinogen concentration that is thought to contribute to hypertension.

2.) Angiotensin receptor blockers and their efficacy in hypertension is similar to that of ACE inhibitors but are associated with a lower incidence of cough. ARB's are preferred for patients who have adverse reactions to ACE inhibitors.

3.) ACE inhibitors not only block the conversion of ANG I to ANG II but also inhibit the degradation of other substances including bradykinin, substance P and enkephalins. The action of ACE inhibitors to inhibit bradykinin metabolism contributes significantly to their hypotensive action. 

4.) Losartan acts at angiotensin AT1 receptors. They also have an effect on AT2 receptors. 

5.) The physiological effect of kinins on veins is contraction and on arteries they cause dilation. Other autacoids like seratonin cause vasoconstriction of the vascular smooth muscle and ergot alkaloids cause vasoconstriction of the blood vessels. 

6.) Bradykinin 2 receptor 

7.) They are not effective as monotherapy in the treatment of  heart failure, however they led to the development of drugs that combine neprilysin 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. 

The combination of an ANG II receptor antagonist with neprilysin inhibitor (ARNI) increases endogenous natriuretic peptide levels while simultaneously blocking the effects of the increase in plasma ANG II. 

8.) Neprilysin is a natural endopeptidase and its inhibition increases bioavailability of natriuretic peptides, bradykinin and substance P which results in natriuretic vasodilatatory and anti-proliferative effects. The effects are prone to produce a powerful ventricular unloading and antihypertensive response. The drug used is sacubitril. 

9.) Endothelium-derived vasodilator is nitric oxide and a endothelium-derived vasoconstrictor is prostaglandin H2.