THE SUPERSENSITIVITY CAUSED BY COCAINE

¹ Department of Pharmacology, Harvard Medical School, Boston, Massachusetts

The intravenous injection of increasing amounts (0.2 to 6.2 mg/kg) of cocaine increased the response of the nictitating membrane of the spinal cat to weak submaximal preganglionic stimulation and to injections of norepinephrine. The responses were potentiated to about the same extent. The response to supramaximal nerve stimulation was little affected by cocaine.

Amounts of cocaine of the same order sensitized the volume change of the spleen of the spinal cat to injected norepinephrine and to nerve stimulation without affecting the amount of sympathin liberated by nerve stimulation. Thus the sensitizing action of cocaine is not due to a reduction of the liberation of sympathin.

The height of the blood pressure response observed on injection of 25 µg/kg norepinephrine into spinal cats was related to the concentration of norepinephrine in the plasma. Cocaine increased both the blood pressure response to norepinephrine and the plasma concentration of norepinephrine without affecting the relationship between these two factors. Cocaine prolonged the half-life of injected norepinephrine. Thus cocaine causes supersensitivity to norepinephrine by delaying its inactivation.

This article has been cited by other articles:

				L. Pradhan, P. A. Dabisch, J. T. Liles, K. C. Agrawal, and P. J. Kadowitz Effect of Acute Intravenous Cocaine Administration on Endothelium-Dependent Vasodepressor Responses to Acetylcholine Journal of Cardiovascular Pharmacology and Therapeutics, March 1, 2003; 8(1): 43 - 51. [Abstract] [PDF]