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87 Cards in this Set
- Front
- Back
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Primary autonomic mechanism for BP homeostasis; involving sensory input from the carotid sinus and aorta to the vasomotor center and output via the parasympathetic and sympathetic motor nerves
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Baroreceptor reflex
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Nerve terminal transporter responsible for recycling catecholamine transmitters after release into the synapse
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Catecholamine reuptake pump
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Storage vesicle transporter that pumps amines from cytoplasm into vesicles
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Catecholamine vesicle pump
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Accelerated HTN causing rapid damage to vessels in end organs; a medical emergency
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malignant hypertension
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Tachycardia resulting from lowering of BP; mediated by the baroreceptor reflex
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Reflex tachycardia
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Mechanism by which diuretics lower BP
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Reduction of blood volume and probably also by a direct vascular effect
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Diuretics most important for treatment of HTN
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Thiazides (eg hydrochlorothiazide) and the loop diuretics (eg furosemide). Thiazides in mild HTN; loops in moderate,severe, and malignant HTN
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Adverse effects of hydrochlorothiazide
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Hypokalemia, slight hyperlipidemia, hyperuricemia, hyperglycemia,
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Adverse effects of furosemide
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Hypokalemia, hypovolemia, ototoxicity
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CV results of sympathoplegics
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Reduction of one or more of the following: venous tone, HR, contractive force of the heart, CO, and total peripheral resistance
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MOA of Alpha2-selective agonists (eg clonidine, methyldopa)
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Cause a decrease in sympathetic outflow by activation of alpha 2 receptors in the CNS
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Methyldopa is a prodrug that converts in the brain to:
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Methylnorepinephrine
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CV effects of Alpha2-selective agonists (clonidine and methyldopa)
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Reduce BP by reducing CO, vasicular resistance or both
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Major compensatory response to Alpha2-selective agonists (clonidine and methyldopa)
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Salt and water retention
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Adverse effect of Clonidine
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Dry mouth, severe rebound HTN if drug is suddenly stopped (can be controlled by reinstitution of clonidine therapy or admin of an alpha blocker such as phentolamine)
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Adverse effect of methyldopa
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Sedation, positive Coombs test, hemolytic anemia
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Reason that the very efficacious nicotinic blockers that act in the ganglia ( hexamethonium and trimethaphan) are now considered obsolete
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Adverse Effects
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Adverse Effects of Ganglion-blocking drugs (Hexamethonium and trimethaphan)
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Toxicities reflect parasympathetic blockade (blurred vision, constipation, urinary hesitancy, sexual dysfunction) and sympathetic blockade (sexual dysfunction, orthostatic hypotension)
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Postganglionic sympathetic nerve terminal blockers
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reserpine, guanethidine
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Drug that depletes the adrenergic nerve terminal of its norepinephrine stores
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Reserpine
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Drug that depletes and blocks the release of the stores of norepinephrine
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Guanethidine
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Major compensatory response to postganglionic sympathetic nerve terminal blockers (reserpine, guanethidine)
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Salt and water retention
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Most serious toxicity of reserpine
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Behavioral depression, which may require discontinuation of the drug (reserpine readily enters the CNS)
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Major toxicities of guanethidine
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Orthostatic hypotension and sexual dysfunction
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Reason cocaine and tricyclic antidepressants interfere w/ the action of guanethidine
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Guanethidine requires the catecholamine reuptake pump to reach its intracellular site of action
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Reason MAO inhibitors were once used in HTN
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They cause the formation of a false transmitter (octopamine) in sympathetic postganglionic neuron terminals and lower BP
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CV effects of Alpha1-selective agents (prazosin)
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reduce vascular resistance and venous return
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Reason nonselective alpha blockers (phentolamine, phenoxybenzamine) are of no value in chronic HTN
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Excessive compensatory responses, especially tachycardia
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Compensatory responses to Alpha1-selective blockers
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salt and water retention, and slight tachycardia
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Adverse effects of alpha1-selective blockers (prazosin)
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Orthostatic hypotension
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CV effects of Beta blockers (eg propranolol)
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Initially reduce CO, but after a few days their action may include a decrease in vascular resistance as a contributing effect (may result from reduced angiotensin levels and B-blockers reduce renin release from the kidney)
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Adverse effects of B-blockers
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Sleep disturbances, sedation, impotence, cardiac disturbances, asthma
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Adverse effects of B-blockers on blood labs
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slightly elevated glucose, LDL, and triglyceride concentrations and diminished HDL levels in the blood
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Vasodilators that work through release of NO from drug or endothelium
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Nitroprusside, hydralazine
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Vasodilators that work through hyperpolarization of vascular smooth muscle through opening of potassium channels
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Minoxidil sulfate, diazoxide
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Vasodilators that work through reduction of calcium influx
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Verapamil, diltiazem, nifedipine
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Vasodilator that works through activation of dopamine 1 receptors
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Fenoldopam
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Toxicities of hydralazine (why it is rarely used)
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Compensatory responses (tachycardia, salt and water retention) and drug-induced lupus
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Extremely efficacious older vasodilator that is a potassium channel opener that hyperpolarizes and relaxes vascular smooth muscle; reserved for severe HTN
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Minoxidil sulfate
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Toxicity of minoxidil
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Severe compensatory responses (marked salt and water retention, marked tachycardia), hirsutism, and pericardial effusion
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Parenteral vasodilators used in hypertensive emergencies
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Nitroprusside and Diazoxide
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Short acting agent that must be infused continuously; MOA involves the release of NO which stimulates guanylyl cyclase and increase cGMP concentration in smooth muscle
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Nitroprusside
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Toxicity of nitroprusside
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Excessive hypotension, tachycardia, and if infusion is continued over several days, accumulation of cyanide or thiocyanate in the blood
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Captopril and enalapril (pril endings) are:
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ACE inhibitors
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SE of ACE inhibitors
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Dry cough, hyperkalemia
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ACE inhibitors are contraindicated in
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Pregnancy and hyperkalemia
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Losartan and valsartan block
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angiotensin receptor
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Angiotensin receptor blockers do NOT cause this SE of ACE inhibitors
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Dry cough
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Block L-type calcium channels
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Calcium Channel blockers
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CCB contraindicated in CHF
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Verapamil
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CCB w/ predominate effect on arteriole dilation
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Nifedipine
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SE of CCB
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constipation, edema and headache
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Reduce heart rate, contractility, and O2 demand
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Beta blockers
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Beta blockers that are more cardioselective
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Beta C2001-selective blockers
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Cardioselective Beta1-blockers:
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Atenolol, acebutolol, and metoprolol
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Beta blockers should be used cautiously in:
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Asthma (bronchospastic effects), diabetes (block signs of hypoglycemia) and peripheral vascular disease
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Non-selective Beta blocker also used for migraine prophylaxis
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Propranolol
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SE of Beta blockers
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Bradycardia, sexual dysfunction, dec in HDL, and increase in TG
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Alpha1 selective blockers
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Prazosin, terazosin, and doxazosin (AZOSIN endings)
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Non-selective Alpha1blocker used to treat pheochromocytoma
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Phenoxybenzamine
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Drug used for rebound HTN from rapid clonidine withdrawal
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Phentolamine
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A1a selective blocker w/ no effects on HTN used for BPH
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Tamsulosin (Flomax)
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SE of alpha blockers
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orthostatic hypotension (esp w/ 1st dose) and reflex tachycardia
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Presynaptic Alpha 2 agonist used in HTN and acts centrally
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Clonidine and methyldopa
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SE of methyldopa
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Positive Coomb's test, depression
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Methyldopa is contraindicated in:
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Geriatrics due to its CNS (depression) effects
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SE of clonidine
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Rebound HTN, sedation, dry mouth
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Direct vasodilator of arteriolar smooth muscle
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Hydralazine
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SE of hydralazine
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Lupus like syndrome
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Arterial vasodilator that works by opening K+ channels
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Minoxidil
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SE of minoxidil
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Hypertrichosis (excessive hair growth on the body)
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IV drug used in hypertensive crisis
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Nitroprusside
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Nitroprusside vasodilates:
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Arteries AND veins
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Toxicity caused by nitroprusside and treatment
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Cyanide toxicity treated w/ sodium thiosulfate
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Thiazide derivative that lacks diuretic properties and works by opening potassium channel; thus hyperpolarizing and relaxing smooth muscle cells
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Diazoxide
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Toxicity of diazoxide
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Hypotension, hyperglycemia, and salt and water retention
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Dopamine D1 receptor activation by this drug causes prompt, marked arteriolar vasodilation, given IV for hypertensive emergencies
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Fenoldopam
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CV effect of ACE inhibitors (eg captopril)
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Reduction in blood levels of angiotensin II and aldosterone and an increase in endogenous vasodilators of the kinin family (bradykinin)
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Toxicity of ACE inhibitors
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cough(30%), renal damage in occasional patients w/ preexisting renal vascular disease (although they protect the diabetic kidney) and renal damage in the fetus (absolutely contraindicated in pregnancy)
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Examples of angiotensin II receptor blockers
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Lasartan, valsartan, irbesartan
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An inhibitor of renin's action on its substrate angiotensinogen; thus reducing the formation of angiotensin I, and in consequence, angiotensin II
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Aliskiren
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Toxicity of Aliskiren
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Headache and diarrhea
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Common AE of Angiotensin antagonists and renin inhibitors
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Reduce aldosteroe levels and cause potassium retention
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Classes of sympathoplegics
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CNS Active agents (clonidine, methyldopa), ganglion blocking drugs, postganglionic sympathetic Nerve terminal blockers (reserpine), and adrenoceptor blockers (Alpha1-selective agents (prazosin) or Beta blockers (propranolol))
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Group that respond better to diuretics and Beta blockers than to ACE inhibitors
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Old Patients
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Group that responds better to diuretics and calcium channel blockers and less well to ACE inhibitors
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Blacks
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Tx of malignant HTN
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Powerful vasodilators (nitroprusside, fenoldopam, or diazoxide) are combined w/ diuretics (furosemide) and Beta Blockers
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