This chapter describes physiological effects of cocaine. In a healthy human, intranasal cocaine increases blood pressure (BP) and activates baroreceptor reflexes, thereby reflexively decreasing sympathetic nerve activity (SNA), the neural stimulus for norepinephrine (NE) release. If there is little stimulus for NE release into the synaptic cleft, there should be little NE available for reuptake by the transporter and thus little transporter activity to be blocked by cocaine. Effects of cocaine on the heart rate, myocardial contractility, and coronary tone are also assumed to be related to inhibition of the cardiac NE reuptake. However, studies in humans challenged this hypothesis because these excitatory effects of cocaine were seen only with the systemic route of administration. Intranasal cocaine increased heart rate and caused α-adrenergic-mediated coronary vasoconstriction in humans, whereas infusion of cocaine directly into the coronary circulation, even at the dose that produced very high local concentration, did not produce the same effects. Treatment of cocaine-induced acute hypertension should be targeted to minimize the increase in cardiac output. Because cocaine causes a sympathetic increase in heart rate, a β-blocker theoretically should be the treatment of choice.
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