Phentolamine (Regitine) is a reversible α1 and α2 blocker used primarily for its vasodilatory effects. When used to control hypertension, one must consider the autonomic effects of blocking these receptors.

Profound vasodilation will lead to hypotension which, in turn, will stimulate baroreceptors (ie, carotid sinus) to decrease vagal (parasympathetic) and increase sympathetic tone on the heart via norepinephrine release. Norepinephrine’s β1 effects will increase heart rate (chronotropy) and contractility (inotropy), but because phentolamine also blocks α2 receptors (normally involved in regulating the release of norepinephrine at the synaptic cleft), the negative feedback loop is lost and potentially even more norepinephrine may be released causing an exaggerated effect of the aforementioned hemodynamic changes (ie, even more tachycardia). For these reasons, I can’t remember the last time I used phentolamine to control blood pressure.

As an intensivist and anesthesiologist, I’ve most commonly seen phentolamine administered as subcutaneous injections surrounding the site of pressor extravasation (especially norepinephrine) into soft tissues from an intravenous line. The idea is that phentolamine will offset the vasoconstrictive effects of pressors to prevent localized tissue damage.

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