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Presented by: Maqzia Mushtaq
Presented to: Sir Abdullah
 Beta receptors are membrane bound G protein
coupled receptors which function primarily by increasing
or decreasing intracellular production of second
messenger cAMP.
 3 types:
 Beta 1 receptors:
 Beta 2 receptors:
 Beta 3 receptors:
located on adipose
tissue.
“PROPRANOLOL”
 Pharmacokinetics:
• Well absorbed orally.
• Low bioavailibility due to high first pass metabolism
in liver.
• Lipophilic in nature so can penetrate into brain easily.
• Metabolism depend on hepatic blood flow.
• Bioavalability is increased when taken just after
meal.
 Pharmacological actions:
Cardiovascular system:
 Dec. heart rate-antianginal
 Dec. force of contraction-antihypertensive
 Membrane stabilizing action-antiarrhythmics
 Reduces ill influence of NA on heart-
cardioprotective.
 Blood vessels:
 Blocks vasodilation and fall in BP evoked by
isoprenaline.
 TPR initially increased (inhibition of vasodilation)-
little change in BP
 On continue treatment resistant vessels gradually
adopt to chronically reduced CO-TPR dec.
 Reduce NA release due to block of presynaptic
beta action
 Dec. renin release from kidney
 Respiratory system:
 Blocking beta 2 in broncial smooth muscle can
cause life threating broncho-constriction in
asthmatics.
 CNS:
 Beside decreasing central sympathetic outflow
causes sedation litharge disturbance in sleep after
long term use.
 Suppresses anxiety.
 Metabolic effects:
 In normal person it has min. effect on basal blood
glucose-long term use dec. insulin.
 Hyperlipidemia-inc. VLDL,TG,CH,LDL.
 Inhibits glycogenolysis in heart,skeletel muscle an in
liver
 Skeletal muscle:
 Inhibit adrenergically provoked tremor.
 Fatigue-reduce blood flow.
 Eye:
 Dec. secretion of aqueous humor-dec. IOT.
 Adverse effects:
 Bradycardia
 Plasma lipid is altered .
 Worsens in asthama.
 Impaired carbohydrate tolerance.
 HTN
 Angina-sudden death
 Cold extremities
 Drug interaction
 digitalis,verapamil causes additive depression of
SA node and AV conduction leading to cardic
arrest.
 Enzyme induces-phenytion,rifampicin, smoking
dec. its plasma conc.
 Cimetidine and hydralazine may increase its
bioavalibility.
 Warning signals of hypoglycemia mediated
through sympathatic stimulation is supressed-
hypoglucemic coma.
 More potent in blocking Beta 1- cardiac receptors.
 Pharmacokinetics:
 Completely absorbed orally.
 Do not cross BBB.
 Daily dose is sufficient because of longer duration
of action.
 Have low lipid solubility.
 Use:
 Atenolol is used in angina and the most
commonly used beta blocker for hypertension.
 Intravenous
It has been used to terminate:
 Peroximal supraventricular tachycardia.
 Episodic atrial fibrillation
 Adrenergically mediated arrhythmia
 Arrhythmia during anaesthesia.
 Intra operative,postoperative hypertension.
 In early treatment of myocardial infarction.
 Both alpha and beta blocker.
 Given as an I.V bolus or infusion in hypertensive
emergencies.
 Actions:
 reduce BP.
 Used in hypertensive emergency.
 Does not alter serum lipid/blood glucose level,
does not cause reflex tachycardia.
 Adverse effects:
 Orthostatic, hypotension ,dizziness
 Use in:
 Hypertension
 Angina pectoris
 Cardiac arrhythmias
 Myocardial infarction
 Congestive heart failure
 Pheochromocytoma
 Migraine
 Anxiety
 Glaucoma
Presentation%202%281%29

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Presentation%202%281%29

  • 1.
  • 2. Presented by: Maqzia Mushtaq Presented to: Sir Abdullah
  • 3.  Beta receptors are membrane bound G protein coupled receptors which function primarily by increasing or decreasing intracellular production of second messenger cAMP.
  • 4.  3 types:  Beta 1 receptors:  Beta 2 receptors:  Beta 3 receptors: located on adipose tissue.
  • 5.
  • 6. “PROPRANOLOL”  Pharmacokinetics: • Well absorbed orally. • Low bioavailibility due to high first pass metabolism in liver. • Lipophilic in nature so can penetrate into brain easily. • Metabolism depend on hepatic blood flow. • Bioavalability is increased when taken just after meal.
  • 7.  Pharmacological actions: Cardiovascular system:  Dec. heart rate-antianginal  Dec. force of contraction-antihypertensive  Membrane stabilizing action-antiarrhythmics  Reduces ill influence of NA on heart- cardioprotective.
  • 8.  Blood vessels:  Blocks vasodilation and fall in BP evoked by isoprenaline.  TPR initially increased (inhibition of vasodilation)- little change in BP  On continue treatment resistant vessels gradually adopt to chronically reduced CO-TPR dec.  Reduce NA release due to block of presynaptic beta action  Dec. renin release from kidney
  • 9.  Respiratory system:  Blocking beta 2 in broncial smooth muscle can cause life threating broncho-constriction in asthmatics.  CNS:  Beside decreasing central sympathetic outflow causes sedation litharge disturbance in sleep after long term use.  Suppresses anxiety.
  • 10.  Metabolic effects:  In normal person it has min. effect on basal blood glucose-long term use dec. insulin.  Hyperlipidemia-inc. VLDL,TG,CH,LDL.  Inhibits glycogenolysis in heart,skeletel muscle an in liver  Skeletal muscle:  Inhibit adrenergically provoked tremor.  Fatigue-reduce blood flow.  Eye:  Dec. secretion of aqueous humor-dec. IOT.
  • 11.  Adverse effects:  Bradycardia  Plasma lipid is altered .  Worsens in asthama.  Impaired carbohydrate tolerance.  HTN  Angina-sudden death  Cold extremities
  • 12.  Drug interaction  digitalis,verapamil causes additive depression of SA node and AV conduction leading to cardic arrest.  Enzyme induces-phenytion,rifampicin, smoking dec. its plasma conc.  Cimetidine and hydralazine may increase its bioavalibility.  Warning signals of hypoglycemia mediated through sympathatic stimulation is supressed- hypoglucemic coma.
  • 13.  More potent in blocking Beta 1- cardiac receptors.  Pharmacokinetics:  Completely absorbed orally.  Do not cross BBB.  Daily dose is sufficient because of longer duration of action.  Have low lipid solubility.
  • 14.  Use:  Atenolol is used in angina and the most commonly used beta blocker for hypertension.
  • 15.  Intravenous It has been used to terminate:  Peroximal supraventricular tachycardia.  Episodic atrial fibrillation  Adrenergically mediated arrhythmia  Arrhythmia during anaesthesia.  Intra operative,postoperative hypertension.  In early treatment of myocardial infarction.
  • 16.  Both alpha and beta blocker.  Given as an I.V bolus or infusion in hypertensive emergencies.  Actions:  reduce BP.  Used in hypertensive emergency.  Does not alter serum lipid/blood glucose level, does not cause reflex tachycardia.  Adverse effects:  Orthostatic, hypotension ,dizziness
  • 17.  Use in:  Hypertension  Angina pectoris  Cardiac arrhythmias  Myocardial infarction  Congestive heart failure  Pheochromocytoma  Migraine  Anxiety  Glaucoma

Hinweis der Redaktion

  1. pharmacology