cardiovascular drugs Flashcards
Regulation of TPR by noradrenaline and RAAS
Noradrenaline -> alpha 1 -> IP3 -> Ca2+ -> constriction
Ang II -> IP3 -> Ca2+ -> constriction
How does SNS increase frequency and force of contraction
Via Beta-1 receptors -> cAMP -> increased Ca2+ -> increased rate/force
How does PNS decrease frequency
Decrease cAMP via M2 receptors
What receptors allow constriction of venules
AT1-R
What allows regulation of TRP
Ang II and Noradrenaline (SNS)
Who to not give an ACE inhibitor to
> 55 years old (give calcium channel blocker)
African Americans
Those with co-existing diseases
Problems with ACE inhibitors
Hyperkalaemia Renal impairment (ACE inhibitor prevents constriction of efferent arteriole - becomes dilated) Prevent substance P and bradykinin being down -> coughing
Angiotensin receptor blockers ARBs - action (tartan ending drugs)
Block actions of Ang II on AT1-R
Minimal side effects
Example of an aldosterone antagonist
Spiralactone
What is primary aldosteronism
A hormonal disorder that leads to high blood pressure
Mechanism of action of Ca2+ channel blockers
Target L type ca2+ channels on smooth muscle of arterioles and relax them
Classes of Ca2+ channel blockers
Dihydropyridines (amlodipine)
Phenylalkylamines (verapamil)
Benzothiazepines (diltiazem)
Side effects of Calcium channel blockers
Peripheral Oedema
Flushing and headaches
Grapefruit juice enhances action
Mechanism of action of thiazide diuretics
Block sodium chloride co transporter in DCT
Sometimes activation of K(ATP) channels - smooth muscle dilation of arterioles decrease BP
Side effects of thiazide diuretics
Hypokalaemia
Increase in urate
Increase in glucose and blood lipids (not used in diabetics)