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Haemodynamic effects of cigarette smoking during chronic selective and non-selective beta-adrenoceptor blockade in
Insights
Cigarette smoking increases blood pressure similarly in patients with essential hypertension, whether or not they are on beta-blockers. However, beta-blockers like propranolol and metoprolol significantly reduce the smoking-induced heart rate increase.
Area of Science:
- Cardiovascular Pharmacology
- Hypertension Research
Background:
- Cigarette smoking is a significant risk factor for cardiovascular disease.
- Essential hypertension management often involves beta-adrenoceptor blockers.
- The interaction between smoking and beta-blockers on haemodynamics requires further elucidation.
Purpose of the Study:
- To investigate the haemodynamic effects of cigarette smoking.
- To assess the impact of chronic propranolol and metoprolol treatment on these effects in hypertensive patients.
Main Methods:
- 16 patients with essential hypertension participated.
- Haemodynamic parameters were measured before and during smoking.
- Measurements were taken during periods with and without chronic beta-blocker medication (propranolol and metoprolol).
Main Results:
- Smoking consistently increased blood pressure to a similar degree across all sessions.
- Heart rate increase during smoking was significantly attenuated by both propranolol and metoprolol.
- Forearm blood flow decreased during smoking in both medication periods.
- Plasma adrenaline levels significantly increased during smoking, while noradrenaline levels remained unchanged.
Conclusions:
- Chronic treatment with selective or non-selective beta-blockers does not significantly alter smoking-induced blood pressure changes in essential hypertension.
- Beta-blockers effectively mitigate the heart rate elevation associated with smoking in these patients.
Abstract:
1 Haemodynamic effects of cigarette smoking before and during chronic treatment with propranolol and metoprolol were studied in 16 patients with essential hypertension. 2 Smoking of cigarettes induced an increase in blood pressure of the same degree in all experimental sessions. Heart rate increased by 16 beats/min during smoking alone, but increased significantly less, when a beta-adrenoceptor blocker was used. Forearm blood flow decreased during smoking in both medication periods. 3 Plasma adrenaline rose significantly during smoking from 0.37 nmol/l to 0.77 nmol/l; plasma noradrenaline did not change. 4 It is concluded that the blood pressure changes induced by smoking are not essentially altered during chronic treatment with selective or non-selective beta-adrenoceptor blockade. Only the increase in heart rate is significantly less pronounced during treatment with both drugs.