1.  In which diseases are angiotensinogen levels increased?  What are the
implications of this?
Hypertension
Corticosteroids, estrogens, thyroid hormones, and ANG II all increase the production of angiotensinogen.

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 block the bradykinin metabolism and bradykinin levels are increased which leads to a common side effect of ACE inhibitors which is a dry cough. 
Angiotensin receptor blockers however, do not influence bradykinin metabolism and therefore no
dry cough is experienced.

3. In which way do ACE inhibitors have a two-fold mechanism of action in the
treatment of hypertension?
ACE inhibitors block the conversion ANG I and ANG II as well as the metabolism of
bradykinin to an inactive metabolite. ANG II leads to an increase in Blood pressure
thus, blocking the conversion of ANG I to ANG II , ACE inhibitors will decrease blood
pressure

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

Losartan and other similar drugs are specific competitive antagonists at angiotensin
AT1 receptors
When ANG II is increased AT2 receptors are receptors.

5. What are the physiological effects of kinins on arteries and veins?  Do other
autacoids play a role in this action?  Explain.
Kinins are potent vasodilators and increase the blood flow in the body.                                       Histamine and Serotonin also play a role in this action.
Histamine - H1 and H2 receptors dilatate blood vessels and capillaries
Serotonin- 5-HT2 receptors for vasoconstricting activity and 5-HT1 for vasodilating activity

6. Which receptor is probably the most involved in the important clinical effects of
kinins?
ß2 Receptors 

7. In which way are natriuretic peptides possibly effective in the treatment of
hypertension, as well as congestive heart failure?
Natriuretic peptides increase sodium and water excretion hence causing vasodilation.
The excretion of sodium and water will decreases the volume of fluid leading to blood pressure decreasing while the vasodilation causes better blood flow and therefore 
reducing blood pressure.

8. What is neprilysin 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 is a neutral endopeptidase and is responsible for degradation of natriuretic
peptides in liver, lungs and kidneys. Neprilysin inhibitors prevent degradation
of natriuretic peptides, increases ANP and BNP and also cause natriuresis and
diuresis.   
A drug used as such is Sacubitril.

Give examples of endothelium-derived vasodilators and vasoconstrictors.
Vasodilators: Nitric oxide and PGI2
Vasoconstrictors: ET1