Cocaine-induced hypertension: role of the peripheral sympathetic system

Pharmacol Res. 1999 Aug;40(2):139-45. doi: 10.1006/phrs.1999.0503.


Cocaine causes hypertension at least in part by stimulating the sympathetic nervous system, but it is not clear if this effect is centrally or peripherally mediated. To address this issue we studied the vasoconstrictive effect of cocaine in vivo and in isolated artery segments. In vivo cocaine increased mean arterial blood pressure (MAP) by 40 mmHg within 1 min of administration. Pretreatment with prazosin blocked this response by 62%. With clonidine the pre-cocaine MAP was lower and the hypertensive effect of cocaine was blocked by 50%, indicating an important role for central alpha-adrenergic mechanisms. In isolated rat carotid arteries cocaine-induced vasoconstriction was completely blocked by prazosin, phentolamine, and 6-hydroxydopamine, indicating a clear role for a peripheral effect. However, the relative contribution of the central alpha-adrenergic mechanism to the total vasoconstrictive response of cocaine was not clarified. 1999 Academic Press.

MeSH terms

  • Adrenergic Agents / pharmacology
  • Adrenergic alpha-Antagonists / pharmacology
  • Animals
  • Blood Pressure / drug effects
  • Carotid Arteries / drug effects
  • Carotid Arteries / innervation
  • Carotid Arteries / physiopathology
  • Cocaine / pharmacology*
  • Hypertension / chemically induced
  • Hypertension / physiopathology*
  • In Vitro Techniques
  • Male
  • Oxidopamine / pharmacology
  • Phentolamine / pharmacology
  • Rats
  • Rats, Sprague-Dawley
  • Sympathetic Nervous System / physiopathology
  • Vasoconstriction / drug effects
  • Vasoconstrictor Agents / pharmacology*


  • Adrenergic Agents
  • Adrenergic alpha-Antagonists
  • Vasoconstrictor Agents
  • Oxidopamine
  • Cocaine
  • Phentolamine