ACE INHIBITORS

Tavishi

Contrary to what Big Playing Cards may claim, ACE inhibitors are NOT an anti-ace card group who are certainly NOT distributing propaganda as such:

Rather, ACE inhibitors are a type of blood pressure medication that works by inhibiting one of the enzymes constituting the renin-angiotensin-aldosterone hormone circuit.

ACE stands for angiotensin-converting enzyme. Angiotensin is a crucial part of the RAAS, which is both a Gujarati folk dance and a critical hormone system. In medical terms, RAAS stands for the renin-angiotensin-aldosterone system.

RAAS: dandiya or kidneys?!

This hormone circuit begins with the release of renin from the juxtaglomerular cells, and ultimately results in an increase in blood pressure. The juxtaglomerular cells are cells within the afferent arteriole which bring blood to the nephron, and are found within the glomerulus, a ball of capillaries.

When blood flow arriving to the nephron is rather lackluster and low, the juxtaglomerular cells convert the protein prorenin to its active form, renin. The active form of renin is proteolytic, and thus cleaves the inactive product angiotensinogen into angiotensin I. Angiotensinogen is a product of the liver.

Angiotensin I is also... useless! Until a nice enzyme called angiotensin converting enzyme comes along and turns it into its active form: angiotensin II. Angiotensin II has some of its own functions, increasing blood pressure by constricting afferent arterioles and stimulates sodium-hydrogen exchangers in the proximal tubules of the nephrons. Then, angiotensin plays the role of... degrading to angiotensin III to stimulate the production of aldosterone! Aldosterone has no crazy functions for any other hormone. Rather, it is produced by the adrenal cortex and results in the reabsorption of solutes like sodium to increase blood pressure.

ACE inhibitors stop RAAS before it gets potent and functional by inhibiting angiotensin-converting enzyme, preventing aldosterone release and the production of angiotensin II. ACE inhibitors are typically used to treat hypertension (fancy word for high blood pressure). The consequential decrease in blood pressure has a variety of other results, including the decrease in cardiac output (lower blood pressure decreases stroke volume, or the amount of blood pumped out during ventricular systole), an increase in sodium in blood (fancy word is natriuresis), increase in bradykinin, and more. ACE inhibitors create both cardiac and urinary effects, which are inseparable purely because of the function of the kidney.

Allow us to focus on the impact of ACE inhibitors on bradykinin.

Bradykinin is a peptide responsible for inflammation and vasodilation. ACE inhibitors additionally inhibit the degradation of bradykinin, resulting in an increase in bradykinin, and creating a characteristic dry cough, and when really dangerous, angioedema. Angioedema is.. not fun. To say the least, it's really really intense and dangerous bouts of swelling. This is one of the most well-known adverse effects of ACE inhibitors. In patients more genetically prone to angioedema, ACE inhibitors are very carefully monitored.

ACE inhibitors are used to treat hypertension, heart attacks, diabetic nephropathy, and more. Diabetic nephropathy may potentially be the most interesting to explore, as it ties in both cardiology and nephrology. Diabetes mellitus is just fancy word for diabetes, and is one of the most common causes of chronic kidney disease. Diabetes mellitus is a condition in which the body is unable to produce insulin, a hormone used to regulate blood glucose. One of the most prominent features of diabetic mellitus in regards to the kidneys is the upregulation of the RAAS, resulting in an increased blood pressure. Because of the increased blood glucose, more glucose is filtered out of the blood, resulting in an upregulation of the sodium glucose cotransporter (takes both sodium and glucose out of the to-be urine and back into the blood). The increased reabsorption of sodium results in the release of renin.

This is one of the many things that ends up leading to CKD and kidney failure as a result of diabetes mellitus- hyperfiltration causes glomerular hypertrophying (is this the participle form..?) and increased glomerular pressure. Nephrons suffer and are very, very sad.

This is where ACE inhibitors come in handy.

captopril!

Now, ACE inhibitors are an entire class of drugs. The most commonly administered ACE inhibitors include benazepril, perindopril, and captopril- the first developed ACE inhibitor! Captopril was synthesized by a Brazilian pit viper! Very smart snake indeed. Jokes aside, an inactive compound functioning as an ACE inhibitor was found in the venom of a Brazilian pit viper, resulting in the creation of captopril!