Activation of -adrenergic receptors promotes vasoconstriction, while the activation of -adrenergic receptors mediates the relaxation of muscle cells, resulting in vasodilation.
The other mechanism is that the alkalosis causes decreased freely ionized blood calcium, thereby causing cell membrane instability and subsequent vasoconstriction and paresthesia.
Like other local anesthetics (such as mepivacaine, and prilocaine), procaine is a vasodilator, and is often coadministered with epinephrine for the purpose of vasoconstriction.
Renin concentration in blood plasma tends to be higher in younger people with hypertension when vasoconstriction may be the main reason for high blood pressure.
As such, an increase in sodium chloride concentration would result in vasoconstriction of afferent arterioles, and reduced paracrine stimulation of juxtaglomerular cells.
It may be stored in crash carts to counteract severe peripheral vasoconstriction secondary to extravasation of peripherally placed vasopressor infusions, typically of norepinephrine.
