Key result
Propranolol caused a marked rise in diastolic and mean blood pressure during smoking, whereas atenolol attenuated systolic blood pressure and tachycardiac responses compared with placebo.
Why the study?
Do selective versus non-selective beta blockers differentially affect the cardiovascular and adrenergic responses to cigarette smoking in healthy volunteers?
RCT (n=7)
Double-blind
Do selective versus non-selective beta blockers differentially affect the cardiovascular and adrenergic responses to cigarette smoking in healthy volunteers?
Selective beta-1 blockers are preferable to non-selective beta blockers in habitual smokers, as non-selective blockade exacerbates smoking-induced increases in blood pressure and vascular resistance.
Answers are grounded in this paper and cite their sources.
Acute smoking raises adrenaline equally despite selective/non-selective beta-blockade; extends mechanistic data but leaves open patient risk implications.
The cardiovascular and adrenergic responses to cigarette smoking during acute selective and non-selective beta adrenoceptor blockade were studied in seven young healthy volunteers in a double blind cross-over fashion. Heart rate, arterial blood pressure, forearm blood flow and plasma levels of adrenaline and noradrenaline were determined before and during the terminal 5 min period of 15 min smoking test. During smoking, plasma concentrations of adrenaline increased markedly and evenly by approximately 0.3 ng/ml in all three experimental sessions. Plasma concentrations of noradrenaline remained unchanged. Propranolol, a non-selective beta blocker, caused a marked rise in diastolic and mean blood pressure and forearm vascular resistance during smoking. This response was not seen in the control series or after selective beta-1 blockage with atenolol. This difference is attributable to propranolol's blockade of adrenaline's vasodilating effect mediated by beta-2 receptors in the resistance vessels. Furthermore, atenolol attenuated the systolic blood pressure and tachycardiac responses induced by cigarette smoking by comparison with placebo. This study suggests that selective beta-1 blockers are preferable in the management of patients who are habitual smokers.
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Trap‐Jensen et al. (1979) conducted an RCT in Healthy volunteers (n=7). Propranolol and atenolol vs. Placebo was evaluated on Cardiovascular and adrenergic responses (heart rate, arterial blood pressure, forearm blood flow, plasma adrenaline and noradrenaline). Propranolol caused a marked rise in diastolic and mean blood pressure during smoking, whereas atenolol attenuated systolic blood pressure and tachycardiac responses compared with placebo.
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