Drug mechanisms

Dihydropryidine mechanism

Blocking L-type Ca2+ channel = no vasoconstriction = decrease BP.  

Dihydropryidine have higher affinity for?

Inactivated state of Ca2+ channel

Verapamil mechanism

Cardioselective drugs bind tighter to the OPEN state of Ca2+ channel  

Verapamil mechanism (specific to dysrhythmia)

Block Ca2+ channel in SA/AV node, where Ca2+ influx mediate phase 0 depolarisation  

Diltiazem mechanism

Cardioselective drugs bind tighter to the OPEN state of Ca2+ channel  

ACEi mechanism

Block ACE / prevent conversion of inactive angiotensin I to active angiotensin II (+III) / prevent activation of angiotensin II type 1 receptor (AT1R)

ARBs mechanism

Competitively antagonise angiotensin II type 1 receptor (AT1R)

Thaizide diuretics mechanism

Block Na+-Cl-cotransporter (NCC), that is supposed to reabsorb Na+/Cl-in the DCT 

Beta blocker mechanism

Antagonist at B1 = reduce HR + force of contraction (therefore reducing CO) / decrease renin secretion

Class II drug mechanism

Block effect of SNS and reduce slope of pacemaker potential in SA node / Reduce rate of SA node firing, decrease HR.

Alpha blocker mechanism

Antagonist at A1 = reduce vasoconstriction  

Statins mechanism

Block cholesterol synthesis in liver by competitively inhibit HMG-CoA reductase  

Ezetimibe mechanism

Blocks absorption of dietary cholesterol by blocking NPC1L1  

Fibrates mechanism

Activate nuclear hormone receptor: PPARs 

GTN mechanism

convert to → NO is an endogenous intracellular signalling molecule that activated soluble guanylyl cyclase: GTP -> cGMP: active PKG

Aspirin mechanism

Irreversible inhibitor of COX -> block production of TXA2 

Clopidogrel mechanism

Irreversible inhibitor of P2Y12 receptor / block action of ADP

Prasugrel mechanism

Irreversible inhibitor of P2Y12 receptor / block action of ADP

Ticagrelor mechanism

Inhibitor of P2Y12 receptor but on allosteric site 

Low mol weight heparin mechanism

Bind to ATIII / able to increase affinity to factor Xa

Dabigatran mechanism

Direct inhibitor of thrombin / block conversion of fribrinogen -> fibrin

Rivaroxaban mechanism

Inhibitor of factor Xa

Lidocaine mechanism

Block inactivate Na+ channels, more prevalent in ischaemic tissue.  

Flecainide mechanism

Open state NaV channel blocker / longer binding duration than lidocaine.

Amiodarone mechanism

Block K+ channel, prolong AP and increase refactory period  

Atropine mechanism

Receptor activation, By subunit open a K+ channel (KACh), leading to K+ efflux from SA node. 

Adenosine mechanism

Lower HR by activation of KACh channels at AV node  

B2 adrenoceptors agonists mechanism

Signal at B adrenoceptor occur via Gs / adenylyl cyclase. Result increase in cAMP / PKA / decrease in cellular Ca2+

Warfin mechanism

Competitive inhibitor of vit K epoxide reductase and prevent recycling of vit K.