ANSWERS 2025
Bosentan - CORRECT ANSWER -
first drug for the antagonism of ETA and ETB (didn't work that well, due to no vasodilation pathways)
main use pulmonary hypertension
Ambrisentan - CORRECT ANSWER -ETA selective theoretically provides an antihypertensive effect
allowed ETB receptors to release NO from endothelial cells
main use pulmonary hypertension
NO nitric oxide - CORRECT ANSWER -NO can be thought of as a vasorelaxant equivalent of ET
NO is released from the endothelial cells into vascular smooth muscle
promotes the activity of guanylate cyclase (sGC) which then promotes cyclic GMP
this reduces intracellular CA2+ resulting in vasodilation
Riociguat - CORRECT ANSWER -
directly stimulates activity of soluble guanylate cyclase (used for pulimary hypertension)
lowering intercellular calcium
Prostacyclin - CORRECT ANSWERV-mainly used for pulmonary hypertension
stimulates AC to produce more cAMP, which reduces intercellular CA2+
therefore prostacyclin relaxes blood vessels in the pulmonary circulation
Endothelial derived hyperpolarizing factor (EDHF) - CORRECT ANSWERV-
Release of EDHF results in opening of calcium channel, and hyperpolarization
hyperpolarization inhibits calcium channel, preventing entry of Ca2+ into the vasscular smooth mussle
resulting in relaxation (dilation over constriction)
Thiazides (group) - CORRECT ANSWERV-most commonly used diretic
Furosemide - CORRECT ANSWER -
Loop diretic (forces people to go to the bathroom alot< high chance that patient stops taking medicatio
n beacuse of this)
Spironolactone - CORRECT ANSWER -K+ sparing diretic prevents potasium loss
Angiotensisn II - CORRECT ANSWER -Binds to the AT1 receptor
main physiological actions include
Aldosterone synthesis and secretion
NaCl reabsorption
Antidiuretic hormone (ADH) release
******vasoconstriction through an increase in Ca2+ in the vascular smooth muscle
Ramipril - CORRECT ANSWER -all ACE inhibitors end in -pril
, inhibits vasoconstriction
inhibits aldosterone secretion (Na retention)
Inhibits NaCL reabsobtion
inhibit ADH release
****increased vasodilation through BK
result Decreased SVR
and an increase in natriuresis and diuresis
Losartan - CORRECT ANSWER -Angiotensing receptor blockers (ARBs)
no effect on bradykinin
less cough
less angioedema
Aliskiren - CORRECT ANSWER -Direct renin inhibitors (DRI)
theory patients 'resistant' to other RAS inhibitors might respond well to DRI
practice DRI has not been popular, first in the line of drugs
Nifedipine - CORRECT ANSWER -(-ipine)
Dihydropyridines act on the vasculature > heart
pharmacodynamics
vasodilation (primary)
arterial>venous
reduces contractility
*****mainly dilates
Verapamil and Diltiazem - CORRECT ANSWER -non-dihydropyridines
both have a greater impact on the heart than dihydropyridines but still, retain vascular effects
pharmacodynamic actions
reduce heart rate
reduce contractility
vasodilation
nifedipine - CORRECT ANSWER -rapid onset calcium blocker
Amlodipine - CORRECT ANSWER -slower onset calcium blocker
Propranolol - CORRECT ANSWER -Beta antagonist blockers
(-lol)
pharmacodynamic actions
decrease heart rate, contractility (b1)
decrease renin secretion (b1)
decrease SNS activity (b1)
reduces BP by reducing cardiac output
and by reducing activation of RAS
Metoprolol - CORRECT ANSWERV-Beta blocker B1
cardioselective
propranolol - CORRECT ANSWERV-Beta blocker B1 and B2