Effect of exercise training in patients with essential hypertension.

The aim of the present study was to examine the effect of regular exercise training in moderate essential hypertension. Twenty subjects (one woman and 19 men) trained for 45 minutes three times a week for 12 weeks, to 60% of their maximal heart rate. Blood pressure was measured at rest and during a maximal exercise test on bicycle ergometer. All subjects achieved training effect measured as a significant reduction in heart rate at comparable submaximal work level and a significant increase in duration of exercise. Diastolic blood pressure at rest decreased from 107 +/- 7 to 101 +/- 5 mmHg (P < 0.01), and at corresponding submaximal exercise level 116 +/- 11 to 106 +/- 11 mmHg (P < 0.01). No significant reduction in systolic blood pressure was found. Exercise training might in some patients with moderate essential hypertension be an alternative to pharmacological treatment.

A comparative study on the effect of atenolol and labetalol on exercise capacity and lipid serum levels in essential hypertension.

Exercise performance was examined in 30 hypertensive subjects (mean age 43.2 +/- 5.4 years) in WHO group I-II, allocated to placebo, atenolol and labetalol treatment during a 3 X 12 weeks' exercise training period. Total work did not show any differences between the placebo and the two treatment periods. Compared to placebo, total cholesterol was reduced by 4.6% (p less than 0.04) in the labetalol and 3.1% (NS) in the atenolol period. Systolic and diastolic blood pressure were significantly reduced both at rest (p less than 0.01) and during exercise (p less than 0.01) in the two drug treatment periods compared to placebo.

Genetic studies of an apoA-I lipoprotein variant.

ApoA-I is the major apolipoprotein component of human high density lipoproteins (HDL). By a 2-D electrophoretic study of serum samples from Norwegian families, an apoA-I variant (apoA-I 2-1) was detected in a healthy individual. In the present study performed to elucidate formal and population genetic aspects of apoA-I, this variant was observed in 4 generations of the family of the propositus. One homozygous individual was found. A codominant autosomal Mendelian inheritance was established for the variant. Two heterozygotes were found among 124 unrelated individuals tested. The apoA-I 2 allele frequency was calculated as 0.008 in this population sample.

Effect of exercise training in patients with essential hypertension.

After 12 weeks of regular exercise training in 34 patients with moderate essential hypertension, supine systolic blood pressure at rest decrease from 152 +/- 2 (means +/- SEM) to 149 +/- 2 mmHg (p less than 0.05), and diastolic blood pressure from 106 +/- 1 to 102 +/- 1 mmHg (p less than 0.001). At corresponding submaximal exercise levels, diastolic blood pressure also decreased significantly from 110 +/- 2 to 98 +/- 3 mmHg (p less than 0.001), but no significant reduction in systolic blood pressure was observed. Heart rate at the same submaximal work load was significantly reduced (p less than 0.01). This data shows that exercise training might have blood pressure lowering effect in patients with moderate essential hypertension, and might in some patients be an alternative to pharmacological treatment.

The two apolipoprotein loci apo A-I and apo A-IV are closely linked in man.

In man the closely linked genes for the apolipoproteins A-I and C-III have been assigned to chromosome 11. Linkage studies performed in a Norwegian family with a mutant apoA-I gene established a close linkage between the loci for apoA-I and apoA-IV. For both sexes combined, the peak lod score was 3.01 at a recombination fraction of 0 = 0.00. Thus this study adds the locus of apoA-IV to the previously reported apolipoprotein gene cluster on chromosome 11. The previously unidentified polymorphic serum protein, USP1, is by immunochemical and electrophoretical methods identified as apoA-IV. ApoA-IV typing should be a valuable tool in elucidating the genomic organization of chromosome 11.

Identification of homozygosity for a human apolipoprotein A-I variant.

An apolipoprotein (apo) A-I variant, previously described in two Norwegian families (Schamaun et al. 1983. Hum. Genet. 64: 380-383), represents a mutation in apoA-I in which a single amino acid substitution of lysine for glutamic acid has taken place at residue 136. An offspring resulting from intermarriage between the two families is genotypically homozygous for this variant. He is the first individual discovered to be homozygous for any of the apoA-I variants. Analysis of lipid data collected from these families indicates one or more lipid abnormalities. The low density lipoproteins (LDL) of subjects having this apoA-I variant demonstrate a compositional abnormality. The plasma cholesterol concentration in the homozygous subject is low because of the extremely reduced levels of LDL and apoB, a property shared by some of his first-degree relatives. However, because of the presence of apoE2 in this family, it is not possible to definitively link these lipid abnormalities to the presence of the A-I variant.