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  1. 1. ANTIHYPERTENSIVE DRUGS a short review Ranjit PandeyRanjit Pandey PharmacistPharmacist ranjitpandey17@gmail.cranjitpandey17@gmail.c omom
  2. 2. Hypertension - Definition  Hypertension can be defined as the level of blood pressure at which there is risk to the organs or vasculature.  Based largely on epidemiological studies.
  3. 3. Hypertension- Definition Category Systolic (mmHg) Diastolic (mm Hg) optimal <120 < 80 normal < 130 < 85 high-normal Hypertension stage 1 stage 2 stage 3 130-139 85-89 140-159 90-99 160-179 100-109 > 180_ >110_
  4. 4. Primary Hypertension - Definition  The category of hypertension when the cause is unknown.  There are probably several different genetic causes as well as a complex interplay of polygenetic and environmental factors.  Includes approximately 90% of cases.  Also referred to as essential hypertension. Even though the underlying cause usually is not known, hypertension can usually be very effectively treated.
  5. 5. Secondary Hypertension - Definition  The category of hypertension when the cause is secondary to renal, endocrine, anatomic disorders etc. Includes approximately 10% of cases.
  6. 6. Hypertension - Clinical Significance 1. Heart disease 2. Stroke 3. Kidney failure 4. Blindness  Effects usually are not apparent until after 10 or more years of sustained high blood pressure.
  7. 7. Treatment Strategies A. Lifestyle Modifications  low fat diet rich in vegetables and fruit  reduction of excess body weight  limited alcohol consumption  daily aerobic exercise  smoking cessation  reduction of sodium uptake B. Drug Therapy
  8. 8. Treatment Strategies . Additional Risk factors for cardiovascular disease smoking dyslipidemia diabetes mellitus age older than 60 sex (men and postmenopausal women) family history of cardiovascular disease
  9. 9. Treatment Strategies Risk Group A  No risk factors  No cardiovascular disease  No Target organ damage Risk Group B  At least one risk factor not including diabetes mellitus  No cardiovascular disease  No target organ damage Risk Group C  Cardiovascular disease  Target organ damage  Diabetes mellitus
  10. 10. Treatment Strategy Blood Pressure Risk group A Risk group B Risk group C High-normal Stage 1 Stage 2 lifestyle modification lifestyle modification lifestyle modification lifestyle modification lifestyle modification (up to 6 months) drug therapy drug therapy drug therapy drug therapy (140-159/90-99) (130-139/85-89) (160-179/100-109)
  11. 11. Blood Pressure Regulation Renin-angiotensin system
  12. 12. Blood Pressure Regulation Sympathetic nervous control
  13. 13. Drugs Used To Decrease Blood Pressure  Very effective at lowering blood pressure Usually do not correct the underlying defect Drug therapy is usually life-long
  14. 14. Diuretics  One of the most common, effective and inexpensive drug classes for the treatment of hypertension.  Several different classes of diuretics are effective including the thiazides, loop diuretics and K+ sparing diuretics.
  15. 15. Diuretics  Inhibit renal tubular reabsorption resulting in a reduction of body salt and water. The mechanism of long-term blood pressure reduction still is not completely clear.
  16. 16. Drugs Acting on the Angiotensin System A. Angiotensin Converting Enzyme (ACE) Inhibitors X
  17. 17. ACE Inhibitors - Mechanism  Inhibit conversion of angiotensin I to angiotensin II  Potentiate actions of bradykinin by inhibiting its degradation bradykinin degradation products ACE (bronchoconstriction)
  18. 18. ACE Inhibitors - Characteristics  Little or no increase in heart rate  Reduces ventricular hypertrophy  Side effects: cough, angioedema and rash  Over-all a very safe class of drugs  Prototype: captopril
  19. 19. Drugs Acting on the Angiotensin System B. Angiotensin Receptor Antagonists  Inhibit the action of angiotensin II by antagonizing one of its receptors  Similar effects as the ACE inhibitors  Lack the effect on the kinins which results in a lower incidence of cough and rash Prototype: losartan
  20. 20. Beta Blockers  Competitively antagonizes the effects of the sympathetic effectors norepinephrine and epinephrine.
  21. 21. Beta Blockers  Blockade of B1-adrenergic receptors in ventricle decreases contractility and the SA node decreases the rate of contraction. Blockade of B-Blockers inhibit renin release which also contributes to a decrease in blood pressure.
  22. 22. Beta Blockers Prototype: propanolol  Side effects: Causes bronchoconstriction due to B-2 receptor blockage.  Over-all well tolerated  Beta blockers should not be discontinued abruptly
  23. 23. Calcium Channel Blockers  Bind to receptors of calcium channels in cardiac and vascular smooth muscle.  Prevent Ca+2 influx into the smooth muscle cells which reduces the contraction of the blood vessels and heart rate.  The different calcium channel blockers differ in their relative effects on vascular and cardiac tissue.
  24. 24. Calcium Channel Blockers Side effects are generally mild. Can cause a reflex increase in heart rate (tachycardia) in response to the vasodilation.  Since they act on arterioles, not veins postural hypotension is rare.  Frequently combined with a B-blocker
  25. 25. Alpha1-Adrenergic Blockers  Alpha1-adrenergic receptors are found on vascular smooth muscle where they mediate vasoconstriction.
  26. 26. Alpha1-Adrenergic Blockers  Side effects: orthostatic (postural) hypotension and reflex tachycardia  Prototype: prazosin.  Blockade of the alpha1-adrenergic receptors results in vasodilation of both the arterial and venous beds .
  27. 27. Alpha1-Adrenergic Blockers  It is usually necessary to take a diuretic with these drugs. B-blockers are also frequently co-administered with these drugs.
  28. 28. Direct-Acting Vasodilators  Directly relaxes the vascular smooth muscle  Several drugs in this category are very quick acting and are mainly used for hypertensive emergencies  Side effects include reflex tachycardia and edema. As a result these drugs are frequently combined with a B-blocker and a diuretic
  29. 29. Direct-Acting Vasodilators  Nitrovasodilators release nitric oxide (NO) activation of guanylate cyclase [cGMP] stimulation of a cGMP-dependent kinase and a decreased cytosolic [Ca+2] relaxation of vascular smooth muscle
  30. 30. Direct-Acting Vasodilators  Several other direct-acting vasodilators that work through poorly defined mechanisms  Examples of nitrovasodilators include nitroglycerin and sodium nitroprusside
  31. 31. Centrally Acting Drugs  Antihypertensive effect results from action in the CNS causing a reduced sympathetic nerve firing rate.  Prototype: clonidine
  32. 32. Centrally Acting Drugs  Clonidine activates alpha2 and imidazoline receptors in the vasomotor center of the medulla which inhibits the sympathetic nervous system.  Considered a second-line drug or for special cases (ie methyldopa in pregnant hypertensive patients).  A reduced heart rate and cardiac output account for reduction in blood pressure.
  33. 33. Centrally Acting Drugs  An advantage of these drugs is that they do not cause postural hypotension  Side effects - hypertensive rebound if there is an abrupt withdrawal -dry mouth, sedation
  34. 34. Additional Considerations  Hypertension during pregnancy poses a risk for both mother and fetus/ preeclampsia. Hypertension is a major risk factor for kidney and cardiovascular problems in patients with diabetes. Early and cost effective approach is needed by doctors because complications are life threatning and treatment may be life long.