From the Guidelines

Cocaine's mechanism of action is primarily through sympathetic nervous system effects, CNS stimulation, and local anesthetic effects.

Sympathomimetic toxidrome: marked by tachycardia, hypertension, hyperthermia, seizures, diaphoresis, and increased psychomotor activity, resulting from catecholamine reuptake inhibition 1
Catecholamine reuptake inhibition: leads to an accumulation of norepinephrine, epinephrine, dopamine, and serotonin, causing CNS and neuropsychiatric symptoms 1
Local anesthetic effects: blocks neuronal sodium channels, leading to slowed conductance during phase 0 of the cardiac action potential, resulting in QRS prolongation and wide-complex tachycardia 1
Cardiovascular effects: increases heart rate and blood pressure, reduces left ventricular function, and increases end-systolic wall stress, leading to increased myocardial demand 1
Coronary vasoconstriction: reduces oxygen supply, inducing myocardial ischemia, and increases the risk of thrombosis 1

Treatment strategies: benzodiazepines, calcium channel blockers, α1-adrenergic receptor antagonists, and nitrates can be used to manage severe cocaine-induced hypertension and chest pain 1
Cardiac arrest management: standard therapy, including agents such as benzodiazepines, calcium channel blockers, and nitroglycerin, can be effective in patients with cardiac arrest associated with cocaine overdose 1

The FDA Drug Labels for cocaine (PO) do not address this question.

From the Research

The mechanism of action of cocaine involves several key processes:

Inhibition of voltage-gated sodium channels, resulting in local anesthetic action by halting electrical impulse propagation 2
Inhibition of monoamine reuptake, particularly dopamine, from the synaptic cleft, leading to an excess of available dopamine for postsynaptic activation 2, 3, 4, 5
Increase in central nervous system synaptic dopamine, primarily by increasing the release of dopamine into the synapse and binding to the dopamine reuptake transporter 5
Stimulation of post synaptic receptors by synaptic dopamine, resulting in euphoria or a "high" 5

Cocaine's impact on neurotransmission is primarily due to its ability to hinder monoamine reuptake, particularly dopamine:

The mesocorticolimbic dopamine system has exclusive importance for the development and maintenance of cocaine addictive behavior 3
Cocaine's inhibiting action on reuptake of released DA is essential but not sufficient for the development and maintenance of addictive behavior 3
The coexistence of functionally antagonistic, inhibiting actions of cocaine on the mesolimbic DA release and reuptake of released DA may be responsible for biphasic fluctuations in DA transmission 3

Cocaine is a sympathomimetic compound with potent local anesthetic properties:

The principal hypothesis accepted to date to explain the sympathomimetic effects of cocaine is that this drug inhibits neuronal monoamine neurotransmitter reuptake by binding to a transporter or uptake site 6
Cocaine increases the effective concentration of neurotransmitter at adrenergic receptor sites, resulting in autonomic actions 6