Prevalence of hypertension in chronic cocaine users.

The association of cocaine and acute hypertension is well known; however, cocaine use has not generally been linked to chronic hypertension. We hypothesized that chronic use of cocaine over time would increase the prevalence of hypertension and that cocaine induced vasoconstriction would result in urine protein leakage, manifested by microalbuminuria. Therefore, we studied a population of predominantly black male patients admitted for addiction treatment whose drug of dependence was cocaine. A urine toxicology screen was considered positive if cocaine was detected within 24 h prior to or during admission to the hospital. A total of 301 patients with normal renal function were observed over their 2 week hospitalization. The majority (62%) of the patients were normotensive regardless of the status of their initial urine toxicology screen. Twenty percent of the population had acutely elevated blood pressure that normalized within 1 day, whereas 18% had blood pressure chronically >140/90 mm Hg (chronic hypertension). Levels of systolic and diastolic blood pressures were examined at age deciles and compared to the NHANES III (Third National Health and Nutrition Examination Survey) data for a predominantly black population. There was no significant difference in blood pressure with age in the cocaine users compared to the NHANES groups. Random urine samples were screened for the presence of microalbuminuria and no significant elevation was detected in any of the samples tested. We conclude that chronic cocaine use is associated with acute but not chronic hypertension in middle-aged black males. Cocaine use does not cause microalbuminuria.

Chemistry of 8-chloroberberine.

8-Chloroberberine (V), obtained by treatment of oxyberberine (I) with phosphorus oxychloride, is a reactive intermediate. Treatment with ammonia, methylamine, n-propylamine, aniline, and p-toluidine furnished the 8-berberinylidene derivatives IV and VII-X. Reaction of V with malononitrile, ethyl acetoacetate, and ethyl malonate anions yielded the 8-berberinylidene derivatives XII-XIV. Acid hydrolysis of XIV gave 8-berberinylacetic acid (XV) whose reduction provided 8-canadinylacetic acid (XVI). Grignard reagents react readily with V. Methylmagnesium iodide, ethylmagnesium iodide, and benzylmagnesium iodide led to 8,8-dimethyldihydroberberine (XVII), 8,8-diethyldihydroberberine (XIX), and the benzyl derivative XX, respectively. Sodium borohydride reduction of XX gave rise to 8-benzylcanadine (XXI).