1. In which diseases are angiotensinogen levels increased? What are the implications of this?
Estrogens, corticosteroids, thyroid hormones, and ANG II all raise angiotensinogen levels. It is increased among women who take estrogen-containing oral contraceptives and in pregnant women. As a result, an increase in plasma angiotensinogen concentration could lead to hypertension.

2.Why do drugs which inhibit the angiotensinogen system by acting on angiotensin receptors have fewer side effects than those that inhibit ACE

ACE inhibitors can cause angioedema and dry cough by increasing the level of bradykinin in the body.

 

3. In which way do ACE inhibitors have a two-fold mechanism of action in the treatment of Hypertension?

ACE inhibitors prevent the conversion of ANG I to ANG II and the degradation of other compounds such as enkephalins, bradykinin, and substance P. As a result, the activity of ACE inhibitors in inhibiting substances like bradykinin helps to reduce blood pressure.

 

4. At which type of angiotensinogen receptor do losartan and similar drugs act? Do they have any effect, direct or indirect, at other angiotensinogen II receptors?

The medications bind to AT1 receptors and, as ANG II levels rise, they bind to AT2 receptors.

5. What are the physiological effects of kinins on arteries and veins?  Do other autacoids play a role in this action?  Explain.

Kinins promote artery vasodilation due to their direct inhibitory impact on arteriolar smooth muscle; however, it can also be mediated through the release of vasodilator prostaglandins or nitric oxide, such as PGE2 and PGI2. Because of the release of venoconstriction prostaglandin PGF 2 alpha or direct activation of venous smooth muscle, kinins causes veins to constrict. Autacoids, such as bradykinin, which is a powerful vasodilator, have a function.

 

6. Which receptor is probably the most involved in the important clinical effects of kinins? Type B2 receptor.

 

7. In which way are natriuretic peptides possibly effective in the treatment of hypertension, as well as congestive heart failure?

For the treatment of congestive heart failure, natriuretic peptides such as ularitide, carperitide, nesiritide, and urodilatin cause natriuresis and vasodilation.

8.What is neprilysin and what is the rationale for inhibiting its action in the treatment of heart failure?

The enzyme neprilysin is involved in the breakdown of natriuretic peptides. The major goal of neprilysin inhibitor therapy in cardiovascular disease was to raise endogenous natriuretic peptide levels, which would result in the vasodilation and natriuresis that these peptides cause.

9. Give examples of endothelium-derived vasodilators and vasoconstrictors. Vasodilators: Nitric oxide and PGI2 Vasoconstrictors: ET 1 and receptor subtypes ETA and ETB