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Cardiovascular Pharmacology - Coggle Diagram
Cardiovascular Pharmacology
Hypertension
Therapeutic strategy: Reduce CO, BV, PVR
BP = CO X PVR
ANS controls: smooth muscle cells, rate & force of heart, exocrine excretion, metabolic processes
a-adrenoceptors agonists - on blood vessels induce vasoconstriction via smooth muscle cells contraction
B-adrenoceptors agonists- on blood vessels (B2-induced) vasodilation through smooth muscle cells relaxation. On heart (direct effect) mainly B1-mediated by increasing rate & force of contraction
B-blockers
N: B adrenoceptor antagonists
A: Non-selective (B1 & B2) & cardio-selective (B1) B-blockers are equally effective in reducing BP
C: inhibit stimulatory effect of adrenaline on heart.
Decrease renin release,
Decrease sympathetic activity,
Decrease cardiac output
S/E: can cause bronchoconstriction (contraindicated in asthmatics). B-blockers can block B2 adrenoreceptors in the lungs, which normally cause bronchodilation.
Uses: Hypertension, Angina, Cardiac Failure
ACE Inhibitors
N: Enzyme inhibitors
A: Block conversion of Ang I to Ang II
C: vasodilation, decrease Na+, decrease peripheral vascular resistance, decrease aldosterone secretion
S/E: Persistent dry cough- ACE inactivates bradykinin (vasodilator), therefore may be due to bradykinin accumulation in lungs
Uses: Hypertension, Cardiac Failure
Diuretics
N: Ion transporter systems blockers
A: Inhibit reabsorption of Na+ & H2O from the nephron into the kidney
C: Cause an increase in excretion of Na+ in urine (Natriuresis), also effect excretion of K+, Mg2+, Ca2+, Cl-
Uses: Management of oedema associated with CV, heart failure, hypertension
Loop Diuretics: block Na+/K+/2Cl- (NKCC2) transporter in the thick ascending loop of Henle (powerful natriuretic effect)
Thiazides: block Na/Cl exchanger (NCCT) in distal convoluted tubule. (NaCl loss can stimulate renin secretion)
Vasodilators
Ca+ channel blockers cause vasodilation
Influx of Ca+ causes vasoconstriction
Calcium Channel Blockers
N: Block L-type Ca2+ channels
A: Decrease Ca entry, Decrease intracellular Ca
C: vascular smooth muscle relaxation, decrease arteriolar pressure (afterload), decrease cardiac contractility
Uses: Hypertension, Angina
Angina Treatment Goals
Increase O2 supply i.e coronary blood flow
Must watch blood/O2 supply & demand
Decrease myocardial O2 needed
Nitrates
N: Pro-drug when metabolised - release Nitric Oxide (NO)
C: Veno-relaxation & reduction in central venous pressure (reduced Preload). Relax Large arteries: reduces central aortic pressure & cardiac afterload. Coronary Vasodilation, increase in coronary flow. Divert blood from normal to ischemic areas of myocardium
Statins
Lipids: cholesterol contributes to atherosclerosis
N: Enzyme inhibitor (HMC CoA reductase inhibitors)
A: Decrease synthesis of cholesterol
C: Decrease hepatic cholesterol synthesis, increase LDL receptor synthesis, increase LDL cholesterol clearance from plasma, decrease plasma LDL
Warfarin
Clotting factors II (pro-thrombin), VII, IX, X contain modified glutamate residues (y-carboxyglutamate).
The modification of the residues (carboxylation) is dependent on active form of Vit. K
N: Warfarin is a Vit. K antagonist (Vit K reductase inhibitor)
A: Warfarin inhibits the reduction of Vit K to its active form
C: Synthesis of clotting factors, is inhibited
Aspirin
C: decreased platelet activation, decreased mortality for CV events
S/E: aspirin inhibits gastric PGE2, GI upset, bleeding
A: prevents production of a platelet agonist (thromboxane)
N: irreversible inhibitor of cyclooxygenase-1
Heparins
A: Binds (through pentasaccharide sequences) to & accelerates action of AT
C: Heparins Enhance inhibition of clotting factor action
N: Anti-thrombin III (AT) catalyst
Low Molecular Weight Heparins (LMWH)
N: Anti-thrombin III (AT) catalyst
A: Binds (through pentasaccharide sequences) to & accelerates action of AT
Chemical filtration enriches for most active pentasaccharide ie. part of heparin (H5)
C: LMW Heparin binds to antithrombin III & inhibits factor Xa