6. Give three examples of pathologies in which there is anupregulation of RAAS. Next to each one explain your reasoning.

7. How would high levels of angiotensin II (Ang II) affectsomeone with hypertension?

Part II – Grandpa’s Medications

“Now, what about your grandfather’s medications? He’s takinglisinopril and furosemide. How do those interact with your RAASsystem on this diagram that you’ve made?” asked Mom.

“My professor, Dr. Sven, did mention how certain medicationsdisrupt the system and lower blood pressure, which is why grandpais on these medications. But I’m not sure what drug classes thoseparticular medications belong to.” Arie picked up her iPhone andsaid, “Hey Siri! What is lisinopril?”

An automated friendly voice boomed, “Lisinopril is a medicationof the angiotensin-converting enzyme inhibitor class used to treathigh blood pressure, heart failure and after heart attacks. Forhigh blood pressure it is usually a first line treatment…”(Wikipedia, Lisinopril, 2020).

“Ah! Lisinopril is an ACE inhibitor, and furosemide is adiuretic. Ok, now I get it. Let me show you how these drugs disruptthe RAAS pathway and lower Grandpa’s blood pressure.”

Questions

1. Explain why ACE inhibitors (ACEi)and angiotensin receptor blockers (ARB) are prescribed to treathypertension and heart failure.

2. A drug that amplifies the effect ofbradykinin would have what effect? What diseases could it beprescribed to treat?

3. Would a patient taking an ARB havethe same vasodilation effect via bradykinin as a patient taking anACE inhibitor?

4. Spironolactone is a drug thatblocks the aldosterone receptor in the renal collecting tubule. Howwould the sodium and potassium levels in the urine change after apatient is placed on spironolactone? Based on these changes, whatare possible metabolic adverse effects of the drug?