The response of plasma catecholamines to intravenous labetalol: a comparison with sodium nitroprusside.
Changes in mean arterial pressure (MAP), heart rate (HR), and plasma concentrations of norepinephrine (NE) and epinephrine were measured in eight hypertensive patients in a supine position after stepwise infusion of incremental sodium nitroprusside doses and intravenous injection of cumulative labetalol doses. Both drugs induced rises in plasma NE concentration that were linearly related to reductions in MAP. For any reduction in blood pressure (BP), however, the rise in plasma NE concentration induced by labetalol was approximately four times that induced by sodium nitroprusside. The difference can be explained by two effects of labetalol: impairment of neuronal NE uptake and beta-adrenergic-receptor blockade, which are known to reduce NE clearance from plasma. After both drugs there was a correlation between changes in HR and changes in BP and a correlation between changes in HR and changes in plasma NE concentration. Slopes of the regression lines for both relationships were less after labetalol than after sodium nitroprusside, presumably because of the beta-adrenergic-blocking properties of labetalol. Multiple-regression analysis indicated that the plasma NE rise was an important determinant of the vasodepressor response to each drug. The greater plasma NE elevation after labetalol may limit its antihypertensive effect.[1]References
- The response of plasma catecholamines to intravenous labetalol: a comparison with sodium nitroprusside. Lin, M.S., McNay, J.L., Shepherd, A.M., Keeton, T.K. Clin. Pharmacol. Ther. (1983) [Pubmed]
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