• In which diseases are angiotensinogen level increased? What are the implication of this?

Hypertension and Heart failure. Angiotensinogen will be converted to angitensin 1, which will then be converted again by ACE to angiotensin I. This stimulates vasoconstriction, increase glomerula hydrostatic pressure, increase blood volume due to fluid retention. 

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

​​​​​​​​​​​​​​It is because ACE inhibits the production of angiotensin I while the drugs that act on the angiotensin receptors only reduce the effect of angiotensin. Therefore the drug that inhibit ACE causes a deceased the breakdown of bradykinin which will then cause vasodilation leading to server dry caugh.

• In which way do ACE inhibitors have a two fold mechanism of action in the treatment of hypertension

​​​​​​​The ACE inhibitors inhibits the production of angiotensin I therefore it causes a decrease in aldesteron from the adrenal cortex which will lead to a decrease in Na reabsorption then water is excreted to reduce blood volume as well as blood pressure. ACE inhibitors also cause a decrease in ADH from the pituitary gland, decreasing water re tension by the kidneys reducing blood pressure. 

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

​​​​​​​Angiotesin i, they have an indrect effect on angiotensin ii receptors.

• What are the phycological effects of kininis on arteries and veins? Do other autocoids play a role in this action? Explain 

​​​​​​​They are potent vasodilators. They increase CAMP,NO,PG and DAG. Histimine have the same effect as it causes the vasodilation of arterioles and precapillary spintchers which decreases blood pressure. Serotonin has a different effect as it causes vasocinstriction. 

• Which receptor is probably the most involved in the important clinical effects of kinin?

​​​​​​​bradykinin 2 receptor 

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

​​​​​​​The natriuretic peptides are released after tension on heart ventricles metabolized by neprylysin. They caused vasodilation which will decrease blood pressure, increase glomerula filtration and sodium ecxretion, decrease sodium reabsorption there decreasing the after load. 

• What is neprylisine and is the rationale for inhibiting its action in the treatment of heart failure? Can you name the drug being used as such? 

​​​​​​​Neprylisine is a neutral endopeptidisa responsible for degradation of natriuretic peptides in the kidney,liver and lungs. It decreases the circulation of ANP. Sacubitril inhibits neprilysin to increase the circulation of ANP and BNP thus causes natriusis and diuresis. ↓ afterload and blood pressure. 

• Give an example of endothelium-derived vasodilators and vasoconstrictors

​​​​​​​​​​​Vasodilatory: Substance P, CGRP, Vasomera 

Vasoconstriction: NPY 

​​​​​​​