Dose-Dependent Effects and Receptors
The sensitivity of beta-adrenergic receptors to epinephrine is higher than that of alpha-receptors. This determines hemodynamic changes depending on the dose administered:
- Low doses: Stimulation of sensitive beta2-receptors predominates. Skeletal muscle blood vessels dilate, total peripheral resistance (TPR) and diastolic pressure decrease, while systolic pressure increases due to cardiac beta1-receptor stimulation.
- High doses: Alpha-receptors are activated. Vasoconstriction occurs in the skin, mucous membranes, and abdominal organs; heart rate and contractility increase; total peripheral resistance and systemic blood pressure rise.
Blood Pressure Dynamics and Metabolism
Rapid intravenous administration causes a four-phase blood pressure response:
- Sharp rise due to increased cardiac output.
- Brief stabilization or drop (reflex bradycardia).
- Secondary pressor rise due to vasoconstriction and renin secretion.
- Residual hypotension due to sustained beta2-vessel stimulation.
Myocardial oxygen demand increases sharply. Epinephrine stimulates lipolysis and glycogenolysis, leading to hyperglycemia, and causes hypokalemia due to active potassium uptake by skeletal muscle.
Clinical Application
The drug's properties determine its key medical indications:
- Anaphylactic shock: First-line treatment to reverse critical hypotension and bronchospasm.
- Bronchial asthma: Relief of acute bronchospasm via subcutaneous administration.
- Local anesthesia: Addition to anesthetic solutions to cause vasoconstriction, reduce systemic absorption, and prolong the anesthetic effect.
- Ophthalmology: Open-angle glaucoma to reduce intraocular pressure.