Beta adrenoceptor antagonism and pressor response to phenylephrine

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Abstract
Patients on .beta.-blockers may experience a potentially harmful blood pressure rise after topical .alpha.-adrenoceptors such as phenylephrine [a nasal decongestant and mydriatic]. The presumed mechanism for this enhanced pressor responsiveness is unopposed .alpha.-adrenoceptor activity. This possibility was investigated in 12 patients with hypertension by infusing increasing i.v. doses of phenylephrine after 2 wk on propranolol, metoprolol or placebo within a randomized, double-blind, crossover study design. Mean (.+-. SE) phenylephrine doses required to increase systolic blood pressure by 25 mm Hg were 4.8 .+-. 0.7, 4.7 .+-. 0.8 and 5.3 .+-. 0.9 .mu.g/kg on propranolol, metoprolol and placebo; these differences are not significant. Baroreceptor-mediated decreases in heart rate during phenylephrine infusion were in the same range: 15.8, 15.6 and 17.4 mm Hg on propranolol, metoprolol and placebo, over baseline heart rate values. In these 12 patients with hypertension, .beta.-blockade did not induce any appreciable enhancement of .alpha.-adrenoceptor activity, suggesting that patients with hypertension who receive .beta.-blockers do not have enhanced pressor responsiveness.

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