Pharmacology Exam II review Part 2

affects the kidney and liver; they will both try to start to regulate your body due to the lack of blood, both of them are "sensory" organs

releases angiteniogen, kidney then releases Renin which leads to antiotensin I, angiotensin converting enzymes (ACE) are then released and leads to angiotensin II

decreases aldosterone secretion, decreases vasoconstriction of arterioles, decreases water reabsorption, reduces symptoms of CHF

Angiotensin Converting Enzyme inhibitor drug

• increase aldosterone secretion which increase sodium/water reabsorption (wherever sodium goes; water follows)
• vasoconstriction of arterioles
• ADH secretion (releases antidiuretic enzyme?) which increases water reabsorption

Angiotension II receptors

blocks angio II from binding to Angio II receptors and the three symptoms of increase in aldosterone secretion, vasoconstriction of arterioles, and ADH secretion

Angiotension receptor blocker (ARB)

usually ACE because it was used first and so we know it is safe and ARB has more side effects

• increase in force of contraction without increase in oxygen consumption
• increase in calcium flux into the cell to block sodium/potassium ATPase
• increase in sodium concentration (sodium/calcium pump to increase calcium in cell)

Cardiac glycoside; Half life is equal to 1.5-2days in urine

Cardiac glycoside; half life is 5-7 days; feces

• increase in BP/vasoconstriction
• increase in vascular resistance
• decrease cardiac output and increase heart rate

• increase ADH by increasing water reabsorption
• increase aldosterone (sodium and water resistor)
• vasoconstriction

• have reverse effects on 3 effects on angiotension II
• ARBS (competively block receptors for Angiotension to take effect)
• Cardiac glycosides

LD50/ED50 ~ 1

the length of action potential

• Thiazide (hydrochlorothiazide (HTz)
• Organic Acid/loop (Lasix)
• decrease sodium and water reabsorption in kidney to facilitate loss of potassium

alpha 1 blockers

Alpha 1 blocker = vasodilator