1. Hypertension , angiotensinogen coverts renin to angiotensin 1 and that binds to angiotensin 2 which releases aldosterone and ADH or peptides through peptidases. it also causes vasoconstriction which increases the blood pressure (hypertension). 

 

2. Drugs which block ACE will also reduce the amount of bradykinin 2. However, drugs which act on angiotensin receptors may not inhibit the breakdown of bradykinin.

 

3. Blocks the conversion of angiotensin 1 to angiotension 2 which decreases angiotension 2 synthesis = vasodilation, decreasing blood pressure. There is a reduction in angiotenisn 2 and ADH as well as Na+. Therefore if aldosterone is decreased the blood pressure will be decreased.

 

4. Angiotensin 2 antagonists 

no effect on type 2 receptors.

 

5. Kinins are potent vasodilators and yes, substance p, neurokinin A/B, CGRP etc.

 

6. Bradykinin 2 receptors.

 

7. They cause vasodilation which decreases blood pressure there by treating hypertension. It also increases glomerular filtration and sodium excretion, decrease renin and sodium reabsorption and the effect of angiotensin and aldosterone.

 

8. Neprylisin metabolises natriuretic peptides ANP and BNP. it is a neutral endopeptidase responsible for the degradation of natriuretic peptides in the kidney, liver and lungs. inhibiting neprilysin increases circulating levels of ANP and BNP which can cause natriuresis and diuresis It increases the protective natriuretic peptides and an example of a neprilysin inhibitor is sacubitril. 

 

9. NO and PGI2 (dilators)

ET1,2,3 and ETA,B (vasoconstrictors)