2.4 cardiovascular pharmacology Flashcards
Please give an overview of the five major drug classes used for the treatment of hypertension
- Beta-Blockers (propranolol, bisoprolol): competetive anatagonsim at Beta-Receptors (supressing the effects of the sympatic nervous system)
- ACE-Inhibitor: peptid mimetic inhibtis ACE in RAAS system
- AT1 receptor blocker: antagonism at the AT1 receptor
- Calcium Channel blockers (amlodipine): antagonists as L-type Ca2+ channels in arterial smooth muscle cells
- Diuretics (loop (furosemide), thiazides (hydrochloridethiazemide, HCT), potassium-sparing (spironolactone)):
higher production of urine through ionic (na,K,Cl) excretion
What is the rationale for using combination therapies as initial therapies of hypertension?
synergistic (low dose) combination of drugs is more effective and better tolerated than high-dose monotherapy
arterial pressure is the result of cardiac output x peripheral resistance, which are two different target systems –> intended drug-drug interaction
When deciding which drug to start with, one has to consider… individual contraindications individual comorbidities (= preferential use of some drugs from some conditions)
Explain the MOA of beta blockers
- Beta-Blockers (propranolol, bisoprolol): competetive anatagonsim at Beta-Receptors in the sympatic nervous system which are normally activated by (nor)epinephrine
–> adrenergic effects turned off (fight or flight) (–> feed, breed, pee, poop),
decraesed heart rate, decreased heart contraction, decreased renal renin production (vasodilation + decreased H2O retention)
cardioselective beta1 blocker or unspecific ones (beta1-3)
Explain the MOA of RAAS blockers
- ACE-Inhibitor: peptid mimetic inhibtis ACE in RAAS system and therefore blocks the conversion of Angiotension I to Angiotensin II leading to less vasoconstiction and aldosterone production and therefore lowering BP
- AT1 receptor blocker: antagonism at the AT1 receptor, on blood vessels, heart tissues, adrenal gland –> decreased production of aldosterone
Explain the MOA of Ca2+ channel blockers
- Calcium Channel blockers (amlodipine): antagonists as L-type Ca2+ channels in arterial muscle cells (decerased Ca2+ influx across cell membranes)
- -> leading to vasodilation and therefore less vascular resistance (withour decrease of cardiac output)
Explain the MOA of diuretics and name the different subgroups
- loop diuretics (furosemide) inhibition of Na/K/Cl co-transporter at loop of henle
- thiazides (hydrochloridethiazemide, HCT) inhibition of the na/cl symporter at the distal tubule
- potassium-sparing (spironolactone) mineralocorticoid receptor antagonism, increased excretion of Na
–> Higher production of urine through ionic (na,K,Cl) excretion (transport mostly inhibited before) leads to decrease in osmotic force of water and therefore more urine –> lowering of blood volume