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20 Cards in this Set
- Front
- Back
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What's the Beta Blocker's prototype drug?
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Isoproterenol
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What's the effect of β-blockers administration on conduction and HR (dromotropy and chronotropy)?
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↓ Automaticity in SA, AV, and Purkinje system by ↓ slope of Phase 4 depolarization
↓ Conduction velocity in atria ↑ refractory period of the AV node |
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What's the effect of β-blockers administration on heart contractility (inotropy)?
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↓ A/V contraction:
↓ L-type Ca2+ current ↓ Ca2+-induced Ca2+ release |
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How do β-blockers decrease the rate of cardiac relaxation?
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↓ Ca2+-ATPase activity by reducing phospholamban phosphorylation
↓ Phosphorylation of Troponin I |
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What's the mechanism of action during adrenergic β-receptor stimulation?
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G protein activation activates adenylyl cylase = ↑cAMP which binds to PKA regulatory units, allowing it to phospor Ca channels = ↑ Ca entry.
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What's the mechanism of action during muscarinic β-receptor stimulation?
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Activates PKA (via g protein coupled), allowing it to phospor PLB (= stims CaATPase to inc Ca reuptake) and Troponin I (causing disassociation from the myofilaments)
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Antiarrhythmic Properties of β blockers?
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Class II: ↓ contractility = ↓ O2 consumption → ↓ incidence of supraventricular and ventricular deleterious arrhythmias
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What are "stabilizing" activities of β blockers? What activity does this contribute to?
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Local anesthetic effects by blocking voltage-dependent Na+ channels (e.g. propranolol)
antiarrhythmic activity |
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Antihypertensive Properties of β blockers?
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No effect in normal patients but ↓ BP in HTN pts, especially after long-term administration
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Postulated Mechanisms for the Antihypertensive Properties of β blockers?
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↓ CO
↓ β1-mediated renin release → ↓ Angiotensin II → ↓ vascular tone and ↓ PR |
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Vasodilation mechanism of β blockers?
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↑ NO
Activation β2 receptors Block α1 receptors Block Ca2+/stimulation K+ channels Antioxidant activity |
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Effects of NO?
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Paracrine:
↓ platelet/leuko agg/adhesion ↓ LDL oxidation ↓ smooth muscle proliferation SM relaxation (enhances CaATPase via cGMP, causes hyperpolarization) |
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Antianginal Properties of β blockers?
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↓ contractility = ↓ O2 consumption = inc cardiac reserve (better match between demands and heart's ability in CAD pts)
Vasodilators can ↓ incidence of vasospastic episodes in CAD pts |
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Pulmonary effects of β blockers?
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Little effect on normal patients
β2 blockers can produce life threatening bronchoconstriction in COPD/asthma patients |
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Effects of β blockers on diabetics?
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β blockers blunt glycogenolysis and glucose mobilization during hypoglycemia in DM I.
(use with caution in diabetics: consider β1-selective antagonist) |
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Metabolic effects of β blockers?
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↓ insulin sensitivity by “Classical” β blockers = bad glycemic index
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Lipid metabolism effects of β blockers?
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↓ hormone-mediated lipase activation and ↓ release free FAs from fat
Non-selectives = ↓ HDL, ↑ LDL and ↑ TG (opposite for β1-selective) |
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Precautions and Contraindications in the use of β blockers?
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COPD/Asthma
Bradycardia Antiarrhythmic drugs (verapamil) Hypoglycemia |
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Why should one avoid rapid withdrawal of β blockers?
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May cause adverse sympathetic rebound effects (e.g. angina attacks). Caused by overexpression of beta receptors due to body's compensation attempts.
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OD symptoms with beta blockers?
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↑ BP (tx: Isoproterenol or α agonist)
Bradycardia (tx: atropine/pacemaker) EKG: ↑ PR interval and Widened QRS Seizures and depression |
