CLASSES DRUGS MECHANISM SE

ACE inhibitor  Ramipiril Inhibiting the enzyme,  Hypotension : first

 Most widely  Lisinopiril ACE : enzyme found on dose hypotention is
prescribed  Perindopril the surface of pulm & prevalent w ACE
cardiovasv med renal epithelia. By inhibitor
blocking ACE, these drugs  Persistent, dry cough :
prevents aldosterone due to pulm kinin
release from the adrenal accumulation
cortex & eliminate Na+ (  Hyperkalemia : ACE
along w/ water ) from the inhibitors promote
kidneys. These two potassium retention
cumulative effects serve  Other effects : fatigue,
to reduce blood vol & nausea, dizziness,
blood pressure. headache
Block conversion of
angiotensin I   Taking these drugs
angiotensin II w/ NSAIDs
increases risk of
renal failure.
Angiotensin II rec  Candesartan Similar mechamism to  Hypotension
antagonist ( ARBs )  Irbesartan ACE inhibitors.  Hyperkalemia
 Used in place of  Losartan Block the action of  Renal failure ( as with
ACE inhibitor where  Telmisartan angiotensin II at the AT1 ACE inhibitor )
persistent, dry receptor.  Cough – though less
cough has become  Angiotensin II likely than with an ACE
unbearable promotes inhibitor
aldosterone secretion
& acts as a vasocons,  Taking these drugs
its blockage reduces w/ NSAIDs
peripheral vasc increases risk of
resistance  lower renal failure.
blood pressure.
Diuretics  Loop diuretic :  Act at the thick  Hypovolemia,
 Promote diuretic & furosemide, ascending limb hypokalemia,
water loss bumetanide metabolic alkalosis,
 Eliminate excess  Thiazide &  Act at the distal hyperurecemia
sodium & water thiazide-like convoluted tubule  Same as SE loop
from body. Some diuretic : diuretic +
classes eliminate bendroflumethia hypercalcemia,
potassium, zide, hyponatremia
increasing risk of hydrochlorothiaz
hypokalemia. ide, indapamide,
 Other drugs such as metalazone
amiloride,  Potassium-  Act at the cortical  Hyperkalemia
spironolactone, sparing diuretic : colleting duct
retain potassium amiloride,
ions – increase the spironolactone
 risk of  Osmotic diuretic  Act at the proximal
hyperkalemia. : manitol tubule
 Carbonic  Act at the proximal
anhydrase tubule
inhibitor :
acetazolamide
Calcium channel  Amlodipine Reduce Ca2+ entry into SE below focus on
blockers  Nifedipine vasc & cardiac cells. This amlodipine & nifedipine :
 Not all Ca2+  Diltiazem reduce intracellular Ca2+  Flushing
channel blockers  Verapamil conc which in turn,  Headache
have ( Amlo & nife used causes relaxation &  Ankle swelling
antihypertensive for hypertension ) vasodil in arterial smooth  Palpitation
effect. ( dilte & vera used muscle. Ca2+ channel  Lightheadedness
Nonetheless, the for control heart rate blockers also reduce  Cough
following drugs / arrythmia ) myocardial contractility in  Shortness of breath
have a significant the heart.
antihypertensive
effect as part of
their clinical action.
B-blockers  Metoprolol Reduce renin secretion  Fatigue
 As  Bisoprolol from the kidney – an  Cold ext
antihypertension +  Labetalol effect ordinarily mediated  Vivid dreams
tx for ischemic  Nebivolol by beta-1 receptor. Recall  Headache
heart disease, that beta-1 rec are  Nausea
chronic heart located mainly in the  Vivid
disease, artrial heart, whereas beta-2 rec dreams/nightmare (
fibrillation, SVT. are mainly located in the propanolol &
smooth muscle of blood metaprolol )
https://pharmafactz.co vessel and the airways.
m/beta-blocker-
mnemonics/
Alpha blockers  Alfuzosin Alpha 1 rec are  Postural hypotension
 To treat  Tamsulosin predominantly found in  Dizziness
hypertension in  Doxazosin smooth muscle, such as  Faintness
resistant with ACE blood vessels or the ( these SE are pronounced
inhibitor, Ca2+ urinary tract. Stimulation after the first dose )
channel blocker & produces contraction &
thiazide diuretic inhibition causes
relaxation. Alpha blockers
are highly selective for
the alpha-1 rec, causing
vasodil & a reduction in
the blood pressure.
Alpha 2 agonist  Clonidine Centrally-acting alpha-2  Sedation
 Rarely used  Methyldopa agonists. These rec are  Dry nasal mucosa
 Usually taken  Moxonidine activated in the brain  Dry mouth
alongside a diuretic which, once activated,  Rebound hypertension
 open peripheral blood  Postural hypotension
vessel around the body,  Headache
reducing blood pressure.  Fatigue
Renin inhibitor  Aliskiren (should Cleaving angiotensinogen  Angiodema
 Renin is protein & not be taken ( hepatic-produced)   Hyperkalemia
enzyme secr by alongside an angiotensin I. ACE covert  Hypotension
kidney angiotensin-rec angiotensin I   Diarrhea
blocker @ ACE angiotensin II causing  Headache
inhibitor in increased secretion of  Dizziness
diabetic pt due aldosterone- increasing
to an increased blood pressure. Renin
risk of stroke, inhibitor are, then, an
hyperkalemia & effective way to block the
kidney effects of angiotensin II &
complication. reduce blood pressure.

 Alisken : harmful
> beneficial
Vasodilator  Sodium  Used in hypertensive  Hypotension
nitroprusside emergency. IV route  Methemoglobinemia
for a rapid onset  Cyanide poisoning
effect.  Bradyarrythmia
 Deploys nitric oxide  Palpitation
for its  Tachyarryhtmia
antihypertensive  Confusion
effect. NO reduce  Dizziness
total peripheral  Renal azotemia
resistance & venous
return. Reduces both
preload & afterload.

 Hydralazine  Used to treat HT in  Headache

( works as a direct- pregnancy-  Tachycardia
acting smooth gestational  Palpitation
muscle relaxant, hypertension.
 Hypotension
working as vasodil in  Also be used in
 Aching/swelling joints
resistance arterioles- hypertensive
 Flushing
decreasing total emergencies where
peripheral resistance symptoms from
& lowering blood hypertension are
pressure. present.