441-antiHTN everything

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jgiantess
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124291
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441-antiHTN everything
Updated:
2011-12-18 03:47:13
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drugs
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pharmacology
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  1. acetazolamide, methazolamide, dorzolamide, brinzolamide
    • weak diuretic: carbonic anhydrase inhibitor
    • Used primarily for glaucoma: blocks CA in ciliary cells to prevent HCO3- secretion into aqueous humor...and reduce Na and H2O transport --> decrease IOP)
    • Also may be used for acute mountain sickness and epilepsy.
    • Very weak diuretic; CA is in luminal membrane of proximal tubule, so by blocking CA, deplete intracellular H+ and Na/H+ exchanger is inhibited so Na+ stays in lumen.
    • but 99% of CA must be inhibited before diuretic activity expressed. Even if it is blocked, not much effect because thick ascending limb can compensate for the less effective proximal reabsorption.
  2. furosemide
    • diuretic: loop-acting
    • @ thick ascending limb, inhibits Na+/K+/2Cl- co-transporter.
    • Inhibits NaCl reabsorption --> increases NaCl, K+, water, Mg2+ and Ca2+ excretion
    • (hypokalemia due to diversion of Na+ to be reabsorbed at distal tubule, where K+ can easily be excreted)
    • can cause hypomagnesemia.
  3. ethacrynic acid
    • diuretic: loop-acting
    • @ thick ascending limb, inhibits Na+/K+/2Cl- co-transporter.
    • Inhibits NaCl reabsorption --> increases NaCl, K+, water, Mg2+ and Ca2+ excretion
    • (hypokalemia due to diversion of Na+ to be reabsorbed at distal tubule, where K+ can easily be excreted)
    • can cause hypomagnesemia.
  4. bumetanide
    • diuretic: loop-acting
    • @ thick ascending limb, inhibits Na+/K+/2Cl- co-transporter.
    • Inhibits NaCl reabsorption --> increases NaCl, K+, water, Mg2+ and Ca2+ excretion
    • (hypokalemia due to diversion of Na+ to be reabsorbed at distal tubule, where K+ can easily be excreted)
    • can cause hypomagnesemia.
  5. hydrochlorothiazide
    • diuretic: thiazide. Diuretic of choice for HTN.
    • @ early distal tubule, inhibits Na+/Cl- co-transporter.
    • Inhibits reabsorption of NaCl, therefore decreasing urinary excretion of Ca2+ by enhancing Na/Ca exchanger at basolateral membrane to bring Na+ into cell and Ca2+ back into blood. Increases diuresis.
    • Also promotes vasodilation (hyperpolarization of smooth muscle, involving EDHF, PGI2, NO).
    • can cause hypokalemia, similar to loop diuretics.
  6. indapamide
    • diuretic: thiazide. Diuretic of choice for HTN.
    • @ early distal tubule, inhibits Na+/Cl- co-transporter.
    • Inhibits reabsorption of NaCl, therefore decreasing urinary excretion of Ca2+ by enhancing Na/Ca exchanger at basolateral membrane to bring Na+ into cell and Ca2+ back into blood.
    • Also promotes vasodilation (hyperpolarization of smooth muscle).
    • can cause hypokalemia, similar to loop diuretics.
  7. metolazone
    • diuretic: thiazide. Diuretic of choice for HTN.
    • @ early distal tubule, inhibits Na+/Cl- co-transporter.
    • Inhibits reabsorption of NaCl, therefore decreasing urinary excretion of Ca2+ by enhancing Na/Ca exchanger at basolateral membrane to bring Na+ into cell and Ca2+ back into blood.
    • Also promotes vasodilation (hyperpolarization of smooth muscle).
    • can cause hypokalemia, similar to loop diuretics.
  8. spironolactone
    • diuretic: potassium-sparing, aldosterone antagonist.
    • @ late distal tubule & collecting duct, competitive antagonist of aldosterone.
    • Competitively inhibits binding of aldosterone to MR (mineralcorticoid receptors), decrease expression of AIP which increase Na+ channels and Na+/K+ ATP-ase and more ATP... therefore increasing Na+, Cl-, water excretion, and decreases K+ and H+ in urine (no more negative lumen voltage from aldosterone-induced increased Na+ conductance).
    • i.e. Na+ not coming into cell, so K+ doesn't have to leave. ===potassium sparing.
  9. eplerenone
    • diuretic: potassium-sparing, aldosterone antagonist.
    • @ late distal tubule & collecting duct, competitive antagonist of aldosterone.
    • Competitively inhibits binding of aldosterone to MR (mineralcorticoid receptors), decrease expression of AIP which increase Na+ channels and Na+/K+ ATP-ase and more ATP... therefore increasing Na+, Cl-, water excretion, and decreases K+ and H+ in urine (no more negative lumen voltage from aldosterone-induced increased Na+ conductance).
    • i.e. Na+ not coming into cell, so K+ doesn't have to leave. ===potassium sparing.
  10. triamterene
    • diuretic: potassium-sparing, non-aldosterone, direct sodium channel inhibitor.
    • @ late distal tubule & collecting duct.
    • Inhibits entry of Na+ from tubule lumen side...decreases electrical potential across membrane which is the driving force for K+ exchange, therefore increases Na+, Cl-, water excretion; decreases K+ in urine.
  11. amiloride
    • diuretic: potassium-sparing, non-aldosterone, direct sodium channel inhibitor.
    • @ late distal tubule & collecting duct.
    • Inhibits entry of Na+ from tubule lumen side...decreases electrical potential across membrane which is the driving force for K+ exchange, therefore increases Na+, Cl-, water excretion; decreases K+ in urine.
  12. mannitol
    • diuretic: osmotic.
    • Increases osmotic pressure in tubules, holds water in as passes down proximal tubule and loop of henle.
    • Blocks 10-15% filtered Na+.
  13. captopril
    • Angiotensin-converting enzyme inhibitor
    • lowers total peripheral resistance and decreases BP
    • inhibits ACE, which converts Angiotensin I to II
    • therefore, decreases ATII-mediated VC --> decreased PVR
    • and decreases aldosterone secretion --> decreased sodium retention and ECF volume
    • and decreases ADH secretion, decreases thirst.
    • May also block degradation of bradykinin (==VD in lungs, fluid --> dry cough)
  14. losartan
    • Angiotensin-II receptor blocker/antagonist
    • lowers total peripheral resistance and decreases BP
    • competitive antagonist of Angiotensin II at AT1 receptors.
    • Prevents: VC sm, aldosterone secretion, release of adrenal catecholamines, thirst, ADH release.
    • More complete inhibition of angiotensin action than ACEI because chymase also makes AngII.
  15. aliskiren
    • direct renin inhibitor.
    • antihypertensive, blocks renin proteolytic activity of ang-> angI. Suppresses whole RAAS system.
    • Also can block compensatory rise in Plasma Renin Activity (due to loss of stimulation fo AT1 receptors of JGC, compensatory increase in renin release).
  16. timolol
    antihypertensive: non-cardioselective B blocker
  17. nadolol
    antihypertensive: non-cardioselective B blocker
  18. bisoprolol
    • antihypertensive: cardioselective B blocker
    • B1 selective at low doses
  19. labetalol
    antihypertensive: mixed B and A antagonism
  20. carvedilol
    antihypertensive: mixed B and A antagonism
  21. acebutolol
    • antihypertensive: B blocking and partial agonist activity
    • lower blood pressure by decreasing cardiac output (B1) and vascular resistance (B2)
  22. pindolol
    • antihypertensive: B blocking and partial agonist activity
    • lower blood pressure by decreasing cardiac output (B1) and vascular resistance (B2)
  23. prazosin
    • antihypertensive: alpha-1 specific blocker
    • Acts at post-synaptic receptors to prevent phosphorylation/activation of myosin light chain kinase and contraction...
    • leads to arteriole and venous sm dilation --> decrease TPR and arteriol pressure.
    • therefore, prevents catecholamine-induced vasoconstriction.
    • Only acts at vascular smooth muscle.
  24. doxazosin
    • antihypertensive: alpha-1 specific blocker
    • newer...gradual onset of action.
  25. sildenafil, tadalafil, vardenafil
    • vasodilator, not used for treatment of hypertension.
    • phosphodiesterase 5 inhibitor, tx erectile dysfunction.
    • Prevents breakdown of cGMP to 5'GMP to sustain effect of NO--> cGMP --> relaxation of smooth muscle of corpus cavernosum and blood vessel --> maintain erection.
    • Sildenafil may be used to treat primary pulmonary HTN alone OR with endothelin receptor antagonists and prostacyclin.
  26. alprostadil
    • vasodilator. prostaglandin E1 analog.
    • Used in tx of erectile dysfunction.
    • Acts locally, directly increases cAMP in smooth muscle --> decrease calcium --> relaxation. No involvement of NO.
    • Initiates erection whether stimulation present or not.
  27. diltiazem
    • Class 4 Antiarrhythmic: Ca2+ Channel Blocker
    • blocks voltage sensitive Ca2+ current during Phase 2 plateau of non-pacemaker myocytes
    • also decreases automaticity and conduction velocity in both SA and AV nodes.
    • Antihypertensive. Calcium Channel Blocker: primary action on conducting tissues.
    • Decreases flow of Calcium through transmission of nerve impulses. Slows generation of action potentials at SA node, slows conduction of action potentials through AV node.
    • decreases conduction, decrease force of contraction.
  28. nifedipine, amlodipine, felodipine, nimodipine
    • antihypertensive.
    • Calcium Channel blocker: primarily act on arterioles.
    • Decrease Calcium entry into smooth muscles, cause relaxation and therefore decrease TPR.
  29. minoxidil
    • antihypertensive, used for severe HTN only.
    • decreases TPR, decreases BP.
    • Opens K+ channel of smooth muscle
    • hyperpolarization
    • decreased Ca2+ entry
    • relaxation of smooth muscle.
    • SE: hypertrichosis.
  30. hydralazine
    • antihypertensive, acts directly on smooth muscle of blood vessels, vasodilation as a result of endothelium-derived relaxing factor --> opens K+ channels or NO generation.
    • decreases TPR, decreases BP.
    • SE: may increase CO...may cause myocardial ischemia...
    • Not used alone, when combined with BB and diuretic, drug is better tolerated.
  31. sodium nitroprusside
    • antihypertensive, mainstay for hypertensive crises
    • DIRECT VD of arteries and veins by releasing NO.
    • NO--> guanylate cyclase --> cGMP --> cGMP-dependent protein kinase inhibits Calcium influx...Myosin fails to be phosphorylated...decreased contraction.= relaxation
    • also: venous pooling (decrease preload) and decrease arteriolar resistance (decrease TPR and BP)
    • May cause cyanide poisoning: therefore, must be administered with sodium thiosulfate.
  32. nitroglycerin (glyceryl trinitrite)
    • antihypertensive, organic nitrite. tx of Angina.
    • Enzymatically converted (in presence of intracellular sulfhydryl groups) to S-nitrosothiol --> NO.
    • Increased NO --> improves coronary blood flow.
    • Large first-pass metabolism. Rapid onset.
  33. isosorbide dinitrate
    • antihypertensive, organic nitrite. tx of Angina.
    • Enzymatically converted (in presence of intracellular sulfhydryl groups) to S-nitrosothiol --> NO.
    • Increased NO --> improves coronary blood flow.
    • Large first-pass metabolism. Rapid onset.
  34. isosorbide mononitrate
    • antihypertensive, organic nitrite. tx of Angina.
    • Enzymatically converted (in presence of intracellular sulfhydryl groups) to S-nitrosothiol --> NO.
    • Increased NO --> improves coronary blood flow.
    • No first-pass, longer duration of action.
  35. Verapamil
    • Class 4 Antiarrhythmic: Ca2+ Channel Blocker
    • blocks voltage sensitive Ca2+ current during Phase 2 plateau of non-pacemaker myocytes
    • also decreases automaticity and conduction velocity in both SA and AV nodes.
    • antihypertensive. Calcium Channel Blocker - primary action at the heart muscles (myocardium), some in conducting tissue.
    • Decrease Calcium entry into heart muscle, decrease cardiac output.
  36. Sotalol
    • Class III antiarrhythmic: K+ channel blocker
    • blocks K+ in plateau phase & blocks repolarization
    • prolongs AP, increases ERP, more risk of TdP
    • Antihypertensive: non-cardioselective beta-adrenoceptor antagonist
    • blocks B1R - less CO, less renin release so fall in angiotensin II levels and decrease in tubular Na reabs.
    • blocks B2R - presynaptically, reduce NE overflow. Also - (bad) - increases risk of bronchoconstriction, peripheral VC, masking of compensatory response ass'd with hypoglyc...etc.
    • SE: dizziness, weakness, fatigue, N/V, diarrhea, brady, TdP, bronchospasm, aggravation of underlying HF
  37. Esmolol
    • Class II antiarrhythmic: B-adrenoceptor antagonist
    • blocks B1 receptor and SNS stimulation, decreases cAMP
    • @ pacemaker cells:
    • 1) decrease slope of Phase 4: opposes adrenaline effect at transient Ca2+ channels
    • 2) decrease slope of Phase 0: inhibits slow L-type Ca2+ channels, decrease HR
    • @ nonpacemaker cells:
    • at Phase 0, blocks inward Na+ current - increase ERP, decrease conduction.
    • Antihypertensive: B1 selective blocker at low doses
    • therefore, less effect on bronchioles
  38. Propranolol
    • Class II antiarrhythmic: B-adrenoceptor antagonist
    • blocks B1 receptor and SNS stimulation, decreases cAMP
    • @ pacemaker cells:
    • 1) decrease slope of Phase 4: opposes adrenaline effect at transient Ca2+ channels
    • 2) decrease slope of Phase 0: inhibits slow L-type Ca2+ channels, decrease HR
    • @ nonpacemaker cells:
    • at Phase 0, blocks inward Na+ current - increase ERP, decrease conduction.
    • Antihypertensive: non-cardioselective beta-adrenoceptor antagonist
    • blocks B1R - less CO, less renin release so fall in angiotensin II levels and decrease in tubular Na reabs.
    • block B2R - presynaptically, reduce NE overflow. Also - (bad) - increases risk of bronchoconstriction, peripheral VC, masking of compensatory response ass'd with hypoglyc...etc.
  39. Metoprolol
    • Class II antiarrhythmic: B-adrenoceptor antagonist
    • blocks B1 receptor and SNS stimulation, decreases cAMP
    • @ pacemaker cells:
    • 1) decrease slope of Phase 4: opposes adrenaline effect at transient Ca2+ channels
    • 2) decrease slope of Phase 0: inhibits slow L-type Ca2+ channels, decrease HR
    • @ nonpacemaker cells:
    • at Phase 0, blocks inward Na+ current - increase ERP, decrease conduction.
    • Antihypertensive: B1 selective blocker at low doses
    • therefore, less effect on bronchioles
  40. Atenolol
    • Class II antiarrhythmic: B-adrenoceptor antagonist
    • blocks B1 receptor and SNS stimulation, decreases cAMP
    • @ pacemaker cells:
    • 1) decrease slope of Phase 4: opposes adrenaline effect at transient Ca2+ channels
    • 2) decrease slope of Phase 0: inhibits slow L-type Ca2+ channels, decrease HR
    • @ nonpacemaker cells:
    • at Phase 0, blocks inward Na+ current - increase ERP, decrease conduction.
    • Antihypertensive: B1 selective blocker at low doses
    • therefore, less effect on bronchioles

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