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• Hypertension


  Sustained systolic blood pressure of greater than 140 mm Hg or a sustained diastolic blood pressure of greater than 90 mm Hg
• Blood pressure categories


  • Normal: <120 systolic and <80 diastolic
  • Prehypertension: 120–139 systolic or 80–89 diastolic
  • Stage I: 140–159 systolic or 90–99 diastolic
  • Stage II: ≥160 systolic or ≥100 diastolic
• Hypertension results from increased vascular tone
• Consequences of elevated blood pressure

  • Cerebrovascular accidents (strokes)
  • Encephalopathy
  • Cerebral hemorrhage
  • Congestive heart failure
  • Myocardial infarction
  • Renal damage
• Arterial blood pressure


  Directly proportional to cardiac output and peripheral vascular resistance
• Mechanisms controlling cardiac output and peripheral resistance

  • Baroreflexes
  • Renin-angiotensin-aldosterone system
• Most antihypertensive drugs lower blood pressure by reducing cardiac output or decreasing peripheral resistance
• Baroreflexes


  1. Baroreceptors in aortic arch and carotid sinuses send fewer impulses to cardiovascular centers

  2. Reflex response of increased sympathetic and decreased parasympathetic output

  3. Vasoconstriction and increased cardiac output

  4. Compensatory rise in blood pressure
• Renin-angiotensin-aldosterone system


  1. Baroreceptors in kidney release renin

  2. Renin converts angiotensinogen to angiotensin I

  3. Angiotensin I converted to angiotensin II

  4. Angiotensin II is a potent vasoconstrictor

  5. Angiotensin II stimulates aldosterone secretion leading to increased sodium reabsorption and blood volume
• Cardiovascular drug classifications


  • Diuretics
  • β-Adrenoceptor-blocking agents
  • Angiotensin–converting enzyme inhibitors
  • Angiotensin II receptor blockers
  • Calcium-channel blockers
  • α–Adrenoceptor-blocking
  • α-/β-Adrenoceptor-blocking agent
  • Vasodilators
  • Cardiac inotropic agents
• Diuretics


  Lower blood pressure initially by increasing sodium and water excretion, decreasing extracellular volume, cardiac output and renal blood flow, and peripheral resistance
• β-Blockers

  Reduce blood pressure primarily by decreasing cardiac output, decreasing sympathetic outflow from CNS, and inhibiting renin release
• Therapeutic uses of β-Blockers

  • Atrial fibrillation
  • Previous myocardial infarction
  • Angina pectoris
  • Chronic heart failure
• ACE inhibitors


  Lower blood pressure by reducing peripheral vascular resistance without reflexively increasing cardiac output, rate, or contractility
• Mechanism of action of ACE inhibitors

  1. Block ACE that converts angiotensin I to angiotensin II

  2. Increase bradykinin, nitric oxide, and prostacyclin production

  3. Decrease aldosterone secretion

  4. Reduce cardiac preload and afterload
• Angiotensin II receptor blockers (ARBs)


  Block AT1 receptors, decreasing the activation of AT1 receptors by angiotensin II, producing similar effects to ACE inhibitors but without increasing bradykinin levels
• Classes of calcium-channel blockers

  • Diphenylalkylamines (e.g. verapamil)
  • Benzothiazepines (e.g. diltiazem)
  • Dihydropyridines (e.g. nifedipine)
• Calcium-channel blockers


  Dilate arterioles but do not dilate veins
• α-Adrenoceptor blockers


  Decrease peripheral vascular resistance and lower blood pressure by causing relaxation of arterial and venous smooth muscle
• α-/β-Adrenoceptor blockers


  Block α1, β1 and β2 receptors, used in gestational hypertension and hypertensive emergencies
• Vasodilators


  Relax vascular smooth muscle primarily in arteries and arterioles by activating potassium channels, inducing hyperpolarization and inhibiting calcium influx
• Cardiac inotropic agents


  Increase the force of cardiac muscle contraction
• Digoxin


  Mechanism of positive inotropic action: inhibits Na+,K+-ATPase leading to increased myocardial Na+ and Ca2+ concentrations, enhancing contractility
• Clinical uses of digoxin

  • Heart failure
  • Antiarrhythmia
• Pimobendan


  Increases myocardial contractility by increasing myofilament sensitivity to Ca2+, used for treatment of congestive heart failure