1. In what disease states were angiotensinogen levels elevated? What are the effects of this?

hypertension. angiotensin synthesis is stimulated by estrogens, angiotensin II, thyroid hormone and glucocorticoid. thus the elevation of angiotensinogen will lead to more glucocorticoids, thyroid hormone, estrogens, and angiotensin II.

Increased  levels of angiotensin can cause the body to retain too much fluid by the release of aldosterone and ADH or to have elevated blood pressure level

 

2. What is the reason why drugs that inhibit the angiotensin system by acting on angiotensin receptors have fewer side effects than those that inhibit ECPs?

 ACE inhibitors blocks the breakdown of kinin, Increased level of kinin is responsible for these side effect; Dry cough increased potassium levels in the blood (hyperkalaemia),Fatigue ,Dizziness from blood pressure going too low,Headaches

 

ARBs specifically bind to AT receptors

3. How do ACE inhibitors have a dual mechanism of action in treating high blood pressure?

 Relaxes arteries and blood vessels by vasodilation. It works by blocking angiotensin II receptors, which are caused by vasoconstriction in blood vessels. Interferes with the body's RAIS. This also regulates the blood pressure of the body.

4.What types of angiotensin receptors do losartan and similar drugs work on? Do they have direct or indirect effects on other angiotensin II receptors?

Losartan is an angiotensin II antagonist that acts on AT1 receptors. Long-term use of the medication can stimulate AT2 receptors.

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

quinines are mediated by specific B1 and B2 receptors. Activation of quinine receptors is particularly important for the treatment of blood pressure regulation. Quinines are vasodilators. There are several autacoids that also play a role, e.g. Eg PGE2 and PGI1, phospholipase A2, chloride transport, etc. It acts as second messenger transducts. Endothelium-derived vasodilates

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

Kinins produce marked arteriolar direction in several vascular beds, including heart and skeletal muscle. The vasodilation may result from a direct inhibitory effect of kinins on arteriolar smooth muscle.  They maybe mediated by the release of NO, vasodilator prostaglandin such PGE₂ and PGI₂

7.which receptor is probably the most involved in the important clinical effects of kinins?

Kinin B2 receptors

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

The excretion of sodium(salt) and water decreases fluid volume, in turn decreasing blood pressure,  vasodilation allow for widening of blood vessels which facilities easier flow of blood, eventually reducing blood pressure.

9.What is neprylisine and what is the rationale for inhibiting its action in the treatment of heart failure? Can you name the drug being used as such? Refer to Study unit 1 where you have also come across this drug

Neprilysin inhibitors are used to treat high blood pressure and heart failure. They work by blocking the action of neprilysin thus preventing the breakdown of natriuretic peptides.Omapatrilat (including entresto and sacubitril/valsartan) is a neprilysin inhibitor, it decreases metabolism of natriuretic peptides and formation of angiotensin II, thus causing vasodilation and increased sodium and water excretion.

10.Give examples of endothelium-derived vasodilators and vasoconstrictors. 

endothelium-derived vasodilators. Bosentan, macitentan. Sitaxsentan, ambrisentan ad  Daglutril

Endothelium-derived vasoconstrictors

• Adrenalin        
• Thrombine      
• Angiotensin II            
• Vasopressinc
• Endotoxin (LPS)        
• Insuline
• Calcium ions