Cocaine-Responsive miRNA and Blood Pressure Elevation
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See related article, pp 752–760
Abuse of cocaine is a major societal problem that crosses the boundaries of user age, sex, race, and ethnicity. Cocaine use has surged since 2011, and nearly one million individuals in the United States initiate cocaine use annually.1 The financial impact of cocaine use in the United States includes costs associated with healthcare services, lost work productivity, and contact with the criminal justice system. Weekly use of cocaine, particularly in older adults, carries a high risk of cerebral and cardiovascular events, with 6800 deaths attributed to cocaine toxicity in 2015.2 The acute cardiovascular effects of cocaine are attributed primarily to block of catecholamine reuptake into central and peripheral sympathetic neurons. The elevated circulating and synaptic norepinephrine increases heart rate and contractility and mediates vasoconstriction and hypertension. Acute norepinephrine-independent effects of cocaine relate to its effect on proteins involved in cardiac signaling, including voltage-gated sodium, calcium and potassium channels, and calsequestrin.3,4 Ultimately, cocaine toxicity may trigger lethal cardiac arrhythmias, myocardial infarction, and stroke.
In addition to acute cardiovascular effects, cocaine use also is implicated in the development of long-term and adverse cardiovascular consequences, including aortic stiffness and hypertension.5 The molecular pathways by which cocaine contributes to these diseases are poorly understood, but recognition of the pathways may allow for therapeutic intervention to lower cardiovascular risk in patients with a history of cocaine use. In this regard, Zhu et al6 provide an intriguing study in this issue of Hypertension, which identifies a cocaine-responsive microRNA in vascular smooth muscle cells (VSMCs) that mediates the development of aortic stiffness and hypertension in mice. For their studies, Zhu et al6 injected mice with cocaine (20 mg/kg IP …