Antihypertensive action of propranolol in man: lack of evidence for a neural depressive effect
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Abstract:
The hypothesis that a neural depressive action is related to the antihypertensive effects of beta blockers has been evaluated in 14 essential hypertensive male patients through the circulatory response to noxious stimuli. The pressor reaction to mental arithmetic was primarily mediated by cardiac stimulation (beta receptors activation), that to cold by vasoconstriction (alpha receptors activation). Arithmetic and cold were tested to separate the effects of peripheral beta blackade from possible neural and other influences. After propanolol (320 mg per day for 3 wk): (1) The baseline pressure was reduced; (2) appearance, peak, and disappearance time of the circulatory reaction to either stimulus was not altered; (3) the pressor effect of arithmetic was decreased in an extent proportional to the reduced rise of cardiac output; and (4) pressure during cold reached the pretreatment levels through an augmented increase of vascular resistance. Our findings indicate that propranolol depresses only the circulatory reactions mediated through beta receptors activation and provide no evidence of effects other than beta blockade.
Insights
Propranolol, a beta blocker, reduces blood pressure by affecting beta-receptor-mediated responses. This study found no evidence of neural depressive actions beyond its known beta-blocking effects in hypertensive patients.
Area of Science:
- Cardiology
- Pharmacology
- Neuroscience
Background:
- Beta blockers are widely used for hypertension.
- Their antihypertensive effects may involve neural mechanisms.
- This study investigated propranolol's effects on circulatory responses.
Purpose of the Study:
- To test the hypothesis that neural depressive action contributes to beta blockers' antihypertensive effects.
- To differentiate beta-receptor-mediated effects from other influences.
Main Methods:
- 14 essential hypertensive male patients were studied.
- Circulatory responses to mental arithmetic (beta-mediated) and cold (alpha-mediated) were assessed.
- Propranolol (320 mg/day for 3 wk) was administered.
Main Results:
- Propranolol reduced baseline blood pressure.
- Reactions to stimuli were not altered in timing.
- The pressor effect of arithmetic decreased, proportional to cardiac output reduction.
- Blood pressure during cold stimulus increased via augmented vascular resistance.
Conclusions:
- Propranolol's effects are limited to beta-receptor-mediated circulatory responses.
- No evidence supports a neural depressive action beyond beta blockade.
- Findings clarify propranolol's mechanism in essential hypertension.
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