Hypertension and Anti-hypertensive Agents Flashcards by Sanisha Lakhani

what is hypertension

high blood pressure
>140 systolic
>90 diastolic

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what is arterial blood pressure

proportional to the product of cardiac output (CO) + total peripheral resistance (TPR)
- CO: product of heart rate and efficiency
- TPR: elastic resistance of vessels + degree of vascular sm contraction
blood pressure can be reduced by:
- reducing CO
- total blood volume
- increasing blood vessel diameter

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effects of sympathetic and parasympathetic activity on cardiac tissue

heart rate:
- increased by symp NS
- decreased by para NS = dominant
contractile force:
- increased by symp NS = dominant
- decreased by para NS
symp NS increases contraction of vascular sm
symp NS increases renin release from kidneys
= sodium + water retention

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what are short term changes in blood pressure carried out by

baroreceptor reflex

stretch sensitive receptors imbedded in walls of carotid sinus/aortic arch => info about state of arterial contraction/relaxation -> delivered to medulla by afferent neurons

medulla send out stimulatory signals to activate symp/para NS => changes in HR/BP

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how to baroreceptors respond to increased BP

baroreceptors activity increases
sympathetic activity decreases
parasympathetic activity increases

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how to baroreceptors respond to decreased BP

baroreceptors activity decreases
sympathetic activity increases
parasympathetic activity decreases

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what are other BP regulators

angiotensin II
vasopressin
prostaglandins
endothelins

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angiotensin II

increases sympathetic response
decreases parasympathetic response
increases H20 retention
acts directly on vascular sm = vasoconstriction

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vasopressin

antidiuretic hormone

increases water retention

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prostaglandins

vasoconstrictive/dilative eicosanoids

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endothelins

vasoconstrictive/dilative

paracrine: made in endothelial cells - act on vascular sm

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renin-angiotensin system

renin is secreted by granular cells ling kidney arterioles in response to:
- Na+ loss
- decreased BP
- sympathetic activity on kidneys
- B agonists
- PGI2
renin converts angiotensinogen > angiotensin I
angiotensin-converting enzyme (ACE) converts
angiotensin I > angiotensin II

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functions of angiotensin II

increases vasopressin = fluid retention from kidney
stimulates thirst
potent vasoconstrictor
acts on CNS - stimulate increased sympathetic outflow (NE)
promotes Na+ retention by increasing aldosterone secretion

= INCREASE BLOOD PRESSURE

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primary hypertension

due to dysfunction of blood pressure regulation mechanisms

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secondary hypertension

due to diseases that inhibit the flexibility of peripheral blood vessels (diabetes, atherosclerosis) //
affect coronary output (coronary artery disease/congestive heart failure)

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diseases aggravated by high BP

atherosclerosis
congestive heart failure
stroke
renal disease
retinal detachment
Alzheimer's

nonpharmacological treatment of high BP

weight reduction
exercise
quit smoking
reduce alcohol 
reduce sodium intake
reduce saturated fat intake
relaxation techniques

drugs used to treat hypertension

diuretics (increase urine)
B-blockers (decrease BP/HR/E)
a1 antagonists
a2 partial agonists
calcium channel blockers
potassium channel activators
ACE inhibitors
angiotensin receptor antagonists

what is the site of diuretic drug action

nephron

symport

coupled transport of 2 or more substance across a membrane in same direction

antiport

2 or more substances exchanged in opposite directions

loop diuretics

inhibit Na+/K+/2Cl- symport by blocking reabsorption of Na+/K+/2Cl-
= flow of water blood to the lumen of Loop of Henle

used to treat hypertension associated with acute pulmonary edema and congestive heart disease

side effects: K+ and Mg2+ loss, uric acid retention

thiazide diuretics

inhibit Na+Cl- symport in endothelial cells that line distal convoluted tubule

same effect as loop diuretics = LESS POTENT
(less absorption of compounds in DCT - treat less severe hypertension)

side effects: K+ and Mg2+ loss, uric acid retention, hyperglycemia, erectile dysfunction

what does K+ loss lead to

cardiac arrhythmias - block repolarisation phase of cardiac contraction

interactions of diuretics with other drugs

diuretics cause decreased lithium excretion via kidneys diuretics increase risk of cardiac glycoside-induced arrhythmias (digoxin) diuretics = less effective when taken with NSAIDs (aspirin)

B-blockers

reduction in cardiac output = competitive antagonism of B1 adrenergic receptors reduction in renin release from kidneys act on CNS - reduce sympathetic outflow PROPANOLOL (nonspecific - acts on B1/2 = block relaxation) Side effects: can worsen asthma/cause heart failure with congestive heart disease patients

a1 antagonists

block vasoconstrictive actions of a1 receptors in vascular sm DOXAZOSIN Side effects: first dose effect hypotension /impotence

a2 agonists

bind to a2 inhibitory autoreceptors in sympathetic neurons and medulla CLONIDINE Side effects: orthostatic hypotension, rebound hypertension

calcium channel blockers

block L-type Ca2+ channels in arterial sm = preventing vasoconstirction VERAPAMIL Side effects: cardiodepression/AV node block potential for many drug-drug interactions - ability to block p-glycoprotein efflux pump

potassium channel activator

sm relaxation = open K+ ATP channels in vascular sm, hyperpolarisation inhibits calcium entry stimulates renin release MINOXIDIL = decrease BP Side effects: stimulates hair growth cause fluid retention (coadministered with a loop diuretic) reflex tachycardia

ACE inhibitors

bind to active site of ACE reversible inhibition of angiotensin II converting enzyme best in patients with high levels of renin CAPTOPRIL Side effects: persistent cough, angioedema, teratogenic toxic drug interactions: increased risk of sudden death when combined with cotrimoxazole = hyperkalemia (K+ loss)

angiotensin II receptors antagonists

blocks binding of angiotensin II to AT1 angiotensin receptors (competitive) LOSARTAN Side effects: hypotension, headaches, GI upset - no cough = stronger than ACE inhibitors

why are most anti-hypertensive drugs used in combination with other bp lowering drugs

reduces dose needed to achieve desired BP allower lower value to be reach as opposed to single drug side effects reduced typical combination: diuretic + antihypertensive

pulmonary hypertension

elevated BP in pulmonary arteries (lungs 02 -> heart ) : pulmonary embolism, COPD, sleep apnea, heart defects, sickle cell anemia, cirrhosis of liver, AIDS treatment: diuretics, cardiac glycosides calcium channel blockers EPOPROSTENOL, AMBRISENTAN, SILDENAFIL

EPROPROSTENOL

prostacyclin: synthetic PGI2 binds to IP receptor = lowers cAMP formation + PKA activation PKA phosphorylates myosin light chain kinase = inhibits sm contraction => vasodilation lowers cytoplasmic Ca2+ blocks release of ET-1

AMBRISENTAN

competitive antagonist of endothelin- ET-1a/b receptors main target\: ET-1a R in sm = vasocontriction visa IP3=mediated Ca2+ release = teratogens

SILDENAFIL

phosphodiesterase V inhibitor phosphodiesterase V converts cGMP > GMP cGMP + NO activate a K+ channel in vascular sm

peripheral vascular disease

caused by atherosclerotic plaques treatment: antiplatelet drugs: ASPIRIN / CLOPIDOGREL cholesterol-lowering drugs: STATINS ACE inhibitors: CAPTOPRIL