Dose-dependent effects and receptors
The sensitivity of beta-adrenergic receptors to adrenaline is higher than that of alpha-receptors. This determines hemodynamic changes depending on the administered dose:
- Low doses: stimulation of sensitive beta2-receptors predominates. Skeletal muscle blood vessels dilate, total peripheral vascular resistance (TPVR) and diastolic blood pressure decrease, while systolic pressure increases due to stimulation of cardiac beta1-receptors.
- High doses: alpha-receptors are activated. Blood vessels of the skin, mucous membranes, and abdominal organs constrict, heart rate and contractile force increase, and total peripheral resistance and systemic blood pressure rise.
Blood pressure dynamics and metabolism
Rapid intravenous administration causes a four-phase blood pressure response:
- A sharp rise due to increased cardiac output.
- Brief stabilization or decrease (reflex bradycardia).
- Secondary pressor rise due to vasoconstriction and renin secretion.
- Residual hypotension due to persistent beta2-vascular stimulation.
Myocardial oxygen demand increases sharply. Adrenaline stimulates lipolysis and glycogenolysis, leading to hyperglycemia, and also causes hypokalemia due to active potassium uptake by skeletal muscles.
Clinical application
The drug's properties determine its key medical indications:
- Anaphylactic shock: first-line treatment that eliminates critical hypotension and bronchospasm.
- Bronchial asthma: relief of asphyxiating attacks via subcutaneous administration.
- Local anesthesia: addition to solutions to constrict blood vessels, reduce absorption, and prolong the anesthetic effect.
- Ophthalmology: open-angle glaucoma to reduce intraocular pressure.
A low dose targets beta receptors (dilates muscle vessels), while a high dose engages alpha receptors (constricts all vessels and raises blood pressure).
Class and exam questions
Why is adrenaline not taken orally?
The drug is degraded in the gastrointestinal tract, so it is used exclusively parenterally (subcutaneously, intramuscularly, intravenously) or topically.
What causes the depressor notch on the blood pressure graph?
The brief drop in pressure during the second phase is associated with reflex stimulation of the vagus nerve in response to a sharp spike in blood pressure.
What are the main side effects and risks associated with its use?
Cardiac rhythm disturbances (arrhythmias), a sharp increase in blood pressure, tachycardia, and headache are possible. The drug is incompatible with inhalation anesthetics due to the risk of severe arrhythmias.
What else to study on this topic
- Characteristics of epinephrine salts (hydrochloride and hydrotartrate) and dosing
- Electrophysiological effects on the heart and risk of arrhythmias
- Effects of adrenaline on GI motility and the genitourinary system (detrusor, uterus)
- Pharmacokinetics: role of COMT, MAO, and neuronal uptake
- Contraindications and drug interactions with halothane
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