In which diseases are angiotensinogen levels increased? What are the implications of this?
Hypertension. High levels of angiotensin lead to high levels of bradykinin that leads to vasoconstriction and ultimately leads to hypertension.
Why do drugs which inhibit the angiotensinogen system by acting on angiotensin receptors have fewer side effects than those that inhibit ACE?
Drugs that inhibit the angiotensinogen system causes a more complete blockage that the ACE inhibitors. Thus there are fewer side effects because there is less bradykinin.
In which way do ACE inhibitors have a two-fold mechanism of action in the treatment of hypertension?
ACE inhibitors prevent the conversion of angiotensin 1 to angiotensin 2 that causes vasodilation. It also causes a decreased amount of aldosterone that will lead to decreased blood pressure.
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?
Blocks angiotensin 2 receptors, they also have action on angiotensin 1 receptors.
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. Yes, Substance P and CGRP.
Which receptor is probably the most involved in the important clinical effects of kinins?
Bradykinin 2 receptors
In which way are natriuretic peptides possibly effective in the treatment of hypertension, as well as congestive heart failure?
They cause vasodilation and thus reduces the blood pressure.
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.
It that metabolizes ANP and BNP and causes an increase in glomerular filtration. This causes a decrease in blood pressure. The name of the drug is Sacubitril.
Give examples of endothelium-derived vasodilators and vasoconstrictors.