Because of atenolol's relatively extensive excretion into breastmilk and its extensive renal excretion, other agents may be preferred while nursing a newborn or preterm infant or with high maternal dosages.[1][2] Infants older than 3 months of age appear to be at little risk of adverse effects from atenolol in breastmilk. Timing breastfeeding with respect to the time of the atenolol dose appears to be of little benefit in reducing infant atenolol exposure because the time of the peak is unpredictable.[3]

All patients attending the outpatient department were screened for hypertension. An attempt was made to correlate presence of hyperinsulinaemia (HI), dyslipidaemia and anthropometric characteristics in these hypertensives. Effect of angiotensin converting enzyme inhibitor (ACEI) and beta blockers on serum insulin was also studied. 85 patients with blood pressure (BP) ≥ 160/90 mm Hg and 94 controls with a BP of < 130/85 mm Hg were studied. All underwent clinical examination, anthropometric measurements (body mass index (BMI), waist hip ratio (WHR), skin fold thickness (SFT) and laboratory investigation (serum insulin, glucose, lipid profile) and post oral glucose load (POGL) for insulin and glucose. Serum insulin was estimated by I(125) radio immuno assay. Patients were randomly divided into group A (Tab enalapril) and group B (Tab atenolol). In 51 patients who completed the study, fasting and POGL insulin and fasting lipid profile were estimated two months after treatment. Mean age of cases was 38.91 years. 50% of patients had stage II hypertension. BMI was increased in 36 cases (42.35%) as compared to 9 in (9.57%) controls. Increased WHR was found in 40 cases as compared to 26 in controls. The SFT was more in cases compared to controls. 47 (55.29%) of 85 cases had abnormal lipid profile as compared to 25 (26.60%) in 94 controls. The fasting and POGL insulin levels (13.85 and 60.05 micro u/ml respectively) in cases were significantly higher than in controls (6.87 and 16.16 micro u/ml respectively). The mean POGL insulin values were much higher in obese compared to non-obese hypertensives. The decrease in mean fasting and POGL insulin values in patients taking ACEI and beta blockers were similar. Abnormal lipid profile was significantly more in cases than controls. Increased total cholesterol (TC), Low density lipoprotein cholesterol (LDLC) and total cholesterol (TC)/high density lipoprotein (HDL) ratio were the most frequent abnormality. The mean insulin (both fasting and POGL) levels were higher in obese hypertensives and those with abnormal lipid profile. Both drugs had equal efficacy in reducing the insulin values.

The metabolic effects of captopril 25 mg twice daily and atenolol 50 mg daily on glucose, insulin and lipids were compared in 83 otherwise healthy mild-to-moderate hypertensive between the ages of 25 and 60 years in a randomised double-blind trial. Hourly glucose and insulin levels were measured during a 2-hour 75 g oral glucose tolerance test at baseline and after 12 weeks of treatment. Lipid profiles including total cholesterol, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, HDL2, HDL3, triglycerides, apoprotein (Apo)A1, ApoB, and Apo(a) were obtained before and after the treatment period. Blood pressure decreased significantly and equivalently in both treatment groups. The glucose and insulin levels and glucose x insulin product at 2 hours after the glucose load increased after 12 weeks of treatment with atenolol compared with the baseline values, but these parameters all decreased after the treatment period with captopril compared with their baseline values. These results indicate an improvement in insulin sensitivity with captopril and a deterioration with atenolol. HDL-cholesterol and HDL3 decreased in the atenolol group but increased in the captopril group. We conclude that captopril has more favourable effects than atenolol on glucose, insulin and lipid metabolism in the treatment of mild-to-moderate hypertension.

A randomized double-blind trial comparing the alpha-adrenergic blocker doxazosin and the beta-adrenergic blocker atenolol was completed by 131 patients with mild to moderate hypertension. Blood pressure and fasting blood lipids were determined at baseline and 4, 12, and 24 weeks of treatment. At entry, plasma lipids and lipoproteins were similar in those patients randomized to doxazosin or atenolol. After 24 weeks of treatment with atenolol, there were significant (P < .05) decreases in high-density lipoprotein cholesterol (HDL-C) and increases in triglycerides and very-low-density triglycerides (VLDL-T). In contrast, doxazosin was associated with significant (P < .05) increases in HDL-C and decreases in triglycerides and VLDL-T. There were no significant differences in HDL apolipoprotein (apo) A-I or low-density lipoprotein apoB between the drugs, but atenolol decreased the ratio of HDL-C to apoA-I, and doxazosin increased this ratio, differences that were statistically significant (P < .002). Neither apoA-I nor apoB concentration at baseline nor apoE phenotype was predictive of the lipid responses during antihypertensive treatment with either drug. Thus, there are significant favorable changes in HDL-C, total triglycerides, and VLDL-T between patients with mild to moderate hypertension and normal plasma lipids when treated with the alpha-blocker doxazosin compared with the beta-blocker atenolol. Plasma lipid or apo concentrations were not predictive of their lipid response during antihypertensive therapy with either of these agents.

To evaluate the differential effects of beta-blockers on serum lipids and apolipoproteins in normolipidaemic and dyslipidaemic hypertensives, 330 patients with mild to moderate essential hypertension were studied 1 month after placebo therapy and 6 months after monotherapy with propranolol (n = 53), atenolol (n = 66), metoprolol (n = 58), pindolol (n = 53), or celiprolol (n = 100). Serum total cholesterol, triglycerides, high density lipoprotein-cholesterol (HDL-C), low density lipoprotein-cholesterol (LDL-C), and apolipoproteins (Apo) A1 and B were measured at baseline and study end. A total of 136 (41.2%) patients were considered normolipidaemic (pretreatment LDL-C < 160 mg.dl-1) and 194 (58.8%) were considered dyslipidaemic (LDL-C > 160 mg.dl-1). Changes in total cholesterol differed between normolipidaemics and dyslipidaemics with propranolol (+13% in normolipidaemics vs -0.5% in dyslipidaemics, P < 0.001), atenolol (+7% vs -2%, P = 0.01), metoprolol (+9% vs -4%, P0.0006), pindolol (+8% vs -9%, P < 0.001), and celiprolol (-1% vs -13%, P = 0.002). HDL-C differed less, with propranolol (-18% vs -13%), atenolol (-6% vs -2%), metoprolol (-2% vs -6%), pindolol (+4% vs +1%), and celiprolol (+9% vs +4%); none of these changes between normolipidaemic and dyslipidaemic patients were statistically significant. LDL-C changes differed the most, with propranolol (+35% vs -1%, P < 0.0001), atenolol (+15% vs -4%, P = 0.001), metoprolol (+12% vs -6%, P = 0.004), pindolol (+12% vs -13%, P < 0.0001), and celiprolol (+3% vs -16%, P = 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Forty-nine patients, with ages ranging from eighteen to seventy years and with mild to moderate primary hypertension (sitting diastolic blood pressure of greater than or equal to 95 mmgH and less than or equal to 115 mmHg) were randomized into a twenty-one-week, double-blind, prospective study to determine the effects of monotherapy of nifedipine GITS (gastrointestinal therapeutic system) versus atenolol on serum lipids, lipid subfractions, apolipoproteins, (apo), and blood pressure (BP). Nifedipine GITS and atenolol significantly reduced blood pressure, but nifedipine GITS reduced sitting and standing systolic BP significantly more than atenolol (p = .001). Sitting and standing heart rate decreased significantly (p = 0.001) during atenolol therapy but did not change significantly during nifedipine GITS therapy. Atenolol increased weight (mean change + 2.2 lb; p = 0.011), but nifedipine GITS decreased weight (mean change - 2.4 lb; p = 0.07). Nifedipine GITS had a more favorable effect on the lipid profile. High density lipoprotein cholesterol (HDL-C) and HDL2 subfractions were increased significantly (p = .001) as were apo A1 (p = 0.037) and apo A2 (p = 0.025). Nifedipine GITS increased HDL3 (NS), reduced triglycerides (TG) (NS), and had no significant effect on total cholesterol (TC) low density lipoprotein cholesterol (LDL-C) and apo B. Atenolol significantly increased serum total cholesterol (p = 0.039) and HDL-C and HDL2 (p = 0.049 and 0.048 respectively). Atenolol increased TG (NS) and apo B (NS) with little change in apo A1 and apo A2. It is concluded that nifedipine GITS had equal or better antihypertensive efficacy than atenolol and had a more favorable effect on the lipid profile. These effects may offer advantages in reducing CHD risk.

The effects on plasma lipids and apoproteins A-I and B of oral administration of doxazosin and atenolol over a 20-week period were studied in 42 patients with mild to moderate essential hypertension. Total plasma cholesterol decreased by 8.9% (P less than 0.01) and LDL cholesterol by 16.9% (P less than 0.01) after 20 weeks' treatment with doxazosin. Total HDL cholesterol and HDL2 cholesterol concentrations increased slightly during doxazosin treatment and the increase in HDL2 level at 4 weeks was statistically significant (P less than 0.05). At 20 weeks, the levels of total HDL cholesterol and HDL2 were significantly (P less than 0.05) lower with atenolol than with doxazosin. The ratio HDL/total cholesterol increased during doxazosin treatment (P less than 0.05 at 4, 12 and 20 weeks). The HDL/total cholesterol ratio was significantly higher after 20 weeks with doxazosin than with atenolol (P less than 0.05). The levels of VLDL cholesterol and triglycerides increased significantly (P less than 0.01) during atenolol treatment. The concentrations of apoproteins A-I and B did not change significantly during treatment with doxazosin or with atenolol but at 20 weeks the ratio of apo A-I to apo B was significantly (P less than 0.05) lower with atenolol than with doxazosin. On the basis of these results, doxazosin would seem to have significant favourable effects on the serum lipid profile.