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To assess the effects of [Beta] blockers on lipids and apolipoproteins in cigarette smokers and nonsmokers, 330 patients with systemic hypertension received 1 month of placebo and 6 months of [Beta]-blocker monotherapy. Serum total cholesterol, triglycerides, high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, and apolipoproteins [A.sub.1] and B were measured. Total cholesterol increased with propranolol (smokers vs nonsmokers, 8 vs 2%); increased for smokers and decreased for nonsmokers with atenolol (8 vs -3%), metoprolol (6 vs -1%) and pindolol (7 vs -6%); and decreased for both groups with celiprolol (-3 vs -10%). HDL cholesterol decreased with propranolol (smokers vs nonsmokers, -8 vs -18%), atenolol (-7 vs -2%) and metoprolol (-12 vs -1%); increased for smokers and decreased for nonsmokers with pindolol (11 vs -2%); and increased for both groups with celiprolol (5 vs 6%). Similar trends were observed with LDL cholesterol and the total/HDL cholesterol ratio. it is concluded that early noncardioselective [Beta] blockers such as propranolol have significant dyslipidemic effects in both smokers and nonsmokers. Cardioselective drugs such as atenolol and metoprolol, or drugs with partial agonist activity such as pindolol, have variable effects. Celiprolol, a new, highly cardioselective [Beta.sub.1] blocker with partial [Beta].sub.2] agonist activity and vasodilatory properties, has favorable effects on lipids and minimizes the dyslipidemic effects associated with smoking. (Am J Cardiol 1991;67:987-992), Beta blocker drugs, used in the control of hypertension (high blood pressure) and other cardiovascular disorders, cause adverse changes in cholesterol and triglyceride levels. This may be one reason that treatment with beta blockers has not been shown to reduce deaths from coronary causes. The newer, cardioselective beta blockers have not been studied as well as the older ones, and their effects on the blood are not well documented. Cigarette smoking, a risk factor for coronary artery disease, may also reduce high-density lipoprotein (HDL, or the so-called 'good') cholesterol. This is the first study to explore the effects of smoking and beta blockers on cholesterol and other lipids (fats) in the blood. Three hundred thirty patients, over one third of whom were smokers, were treated with one of five beta blockers. The older drugs, such as propranolol, have a strong adverse effect on almost all serum lipids, with a more pronounced effect in smokers. The more selective beta blockers, such as atenolol and metoprolol, have more moderate effects among smokers, and are neutral among nonsmokers. Pindolol is almost neutral among smokers, and has some beneficial effects for among nonsmokers. Celiprolol, a newer and highly selective drug, has consistently favorable effects on lipid profiles among both smokers and nonsmokers. Male smokers with high blood pressure have a threefold increase in the incidence of coronary artery disease, and the results of this study indicate that antihypertensive therapy itself may contribute to this. Whether and to what extent a drug causes adverse effects depends on the pharmacological properties of the drug. Celiprolol had the most beneficial effect of the five drugs in this study. (Consumer Summary produced by Reliance Medical Information, Inc.)