Cocaine Constrictor Mechanisms of the Cerebral Vasculature

Journal of Cardiovascular Pharmacology
Robert M RapoportMario Zuccarello

Abstract

Cocaine constriction of the cerebral vasculature is thought to contribute to the ischemia associated with cocaine use. However, the mechanisms whereby cocaine elicits relevant vasoconstriction remain elusive. Indeed, proposed intra- and intercellular mechanisms based on over 3 decades of ex vivo vascular studies are, for the most part, of questionable relevancy due to the generally low contractile efficacy of cocaine combined with the use of nonresistance-type vessels. Furthermore, the significance attached to mechanisms derived from in vivo animal studies may be limited by the inability to demonstrate cocaine-induced decreased cerebral blood flow, as observed in (awake) humans. Despite these apparent limitations, we surmise that the vasoconstriction relevant to cocaine-induced ischemia is elicited by inhibition of dilator and activation of constrictor pathways because of cocaine action on the neurovascular unit (neuron, astrocyte, and vessel) and on vessels outside the unit. Furthermore, previous cocaine exposure, that is, conditions present in human subjects, downregulates and sensitizes these dilator and constrictor pathways, respectively, thereby enhancing constriction to acute cocaine. Identification of specific intra- and...Continue Reading

References

Apr 12, 2016·International Journal of Cardiology·SeongHun YoonRobert M Rapoport
Nov 11, 2020·Scientific Reports·Nazzareno CannellaRainer Spanagel

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Related Concepts

Microvascular Network
Ischemia
Study
In Vivo
Cerebral Blood Flow Imaging
Biochemical Pathway
Atrial natriuretic factor prohormone (31-67)
Research Subject
Pathologic Vasoconstriction
Blood Vessel

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