2: Lecture 1 Flashcards
What is Hypertension?
*When blood pressure is too HIGH
*Entry point of cardiovascular disease
*Can be asymptomatic
Broad treatment for Hypertension
*Sympathoplegic drugs
*Diuretics
*Vasodilators
*Angiotensin antagonists
What is Myocardial Ischemia?
Heart is not receiving enough oxygen
Broad treatment for Myocardial Ischemia
*Lipid lowering drugs
*Anti-coagulants
*Anti-platelet drugs
What is Heart Failure?
*Systemic tissues not receiving enough oxygen
*Endpoint of myocardial ischemia and hypertension
*Form of systemic ischemia
Broad Treatment for Heart Failure
*Nitrites
*Calcium Channel blockers
*Diuretics
*Angiotensin Antagonists
*Beta-blockers
*Beta-receptor agonists
*Cardiac glycosides
Signaling of Parasympathetic nervous system
Acetylcholine (aCh) on muscarinic receptors of smooth and cardiac muscle
Signaling of Sympathetic nervous system
Adrenaline and Noradrenaline on alpha and beta adrenergic receptors on smooth and cardiac muscle
Function of Parasympathetic nervous system
Slows down heart rate
Function of Sympathetic nervous system
Accelerates heart rate AND increases blood pressure
Location and function of alpha-1 adrenergic receptor
Located: in peripheral blood vessels
Function: increase blood pressure
Location and function of alpha-2 adrenergic receptor
Located: in CNS
Function: regulates release of adrenaline
Location and function of beta-1 adrenergic receptor
Located: in smooth and cardiac muscle (main adrenergic receptor in the heart)
Function: increase heart rate and contractility
Location and function of beta-2 adrenergic receptor
Located: in smooth and cardiac muscle (main adrenergic receptor in the trachea)
Function: causes bronchodilation (upon activation)
Cause and Solution to hypertension
Caused by excess sympathetic activity
Solution is antihypertensive drugs which target the sympathetic nervous system directly (not the parasympathetic nervous system)
Mechanism of increase in Resistance
Increasing alpha-1 adrenergic activity (blood vessels)–>increases constriction of arterioles–>higher blood pressure
BP = CO x increased peripheral vascular resistance
Mechanism of increase in Capacitance
Capacitances–>ability of veins to store blood
Increasing capacitance–>increases amount of blood in capacitance venules–>decreases venous return–>decrease blood pressure
BP = decrease CO (more blood stored in venules) x peripheral vascular resistance
Mechanism of increase in Cardiac Output
Increasing beta-1 adrenergic activity (in heart)–>increases contractility and heart rate–>increases blood pressure–>increases cardiac output
Mechanisms of increase in blood Volume
Regulated by renin-angiotensin-aldosterone system (in kidney)
increased angiotensin II–>increases peripheral blood vessel constriction and resistance (also stimulates aldosterone release by adrenal glands
increased aldosterone–>decrease in diuresis (increase in water reabsorption)–>increases blood volume–>increases blood pressure
Very slow process
