We investigated the effects of alcohol restriction on ambulatory blood pressure (BP), heart rate, and heart rate variability in 33 Japanese male volunteers (37 +/- 1 years, mean +/- SE), who were all habitual drinkers. Subjects were told either to keep their usual drinking habits for 3 weeks (usual alcohol period), or to reduce alcohol intake by at least half of their usual drinking amount (reduced alcohol period). The ambulatory BP, heart rate, and electrocardiographic R-R intervals were measured during a 24-h period with a portable recorder on the last day of each period. A power spectral analysis of R-R intervals was performed to obtain the low-frequency (LF) and high-frequency (HF) components. The percentage of differences between adjacent normal R-R intervals >50 msec (pNN50) was also calculated. The amount of ethanol intake was significantly reduced from 70 +/- 5 mL/day in the usual alcohol period to 19 +/- 3 mL/day in the reduced alcohol period (P < .0001). The daytime systolic BP was significantly lower in the reduced alcohol period than in the usual alcohol period by 4 +/- 1 mm Hg (P < .05). The daytime and nighttime heart rate was significantly lower in the reduced alcohol period than in the usual alcohol (P < .001 for each). The pNN50 and the HF component were significantly higher in the reduced alcohol period than in the usual alcohol period (P < .0001 for each). The LF/HF ratio was significantly lower in the reduced period than in the usual period (P < .01). These results demonstrate that 3-week alcohol restriction produced reductions in ambulatory systolic BP, heart rate, and the index of sympathovagal balance, and augmentations of parasympathetic indices of heart rate variability in Japanese male drinkers.
The effects of alcohol intake on haemodynamics and heart rate variability were investigated with relation to genotypes of aldehyde dehydrogenase 2 (ALDH2), which were determined in 33 male Japanese volunteers (mean +/- s.e., 35.7 +/- 1.4 years) using the PCR-RFLP method. On the alcohol intake day, they consumed 660 ml of beer containing 33 ml of ethanol (0.3-0.5 g/kg of body weight) from 18.00 to 18.30. On the control day, they ingested the same amount of non-alcoholic beer. Ambulatory blood pressure, heart rate, and ECG R-R intervals were measured during a 24-h period with a portable recorder. A power spectral analysis of R-R intervals was performed to obtain the low-frequency (LF) and high-frequency (HF) components. Sixteen subjects were homozygotes for the normal ALDH gene (active ALDH2), only one was a homozygote for the mutant ALDH2 gene (inactive ALDH2), and the remaining 16 were heterozygotes (inactive ALDH2). Alcohol intake did not change 24-h average blood pressure (BP) either in the active ALDH2 group or in the inactive ALDH2 group. However, during the time interval from 18.30 to 0.00, alcohol intake significantly decreased diastolic BP in the active ALDH2 group and both systolic and diastolic BPs in the inactive ALDH2 group. In the active ALDH2 group, alcohol intake did not change heart rate, while in the inactive ALDH2 group, alcohol intake significantly increased 24-h average heart rate by 5.3 +/- 1.6 beats per minute (P < 0.01). In the active ALDH2 group, neither the LF nor the HF component was changed by alcohol intake, while in the inactive ALDH2 group, both the LF and the HF components were significantly decreased during the time interval from 18.30 to 0.00. These results demonstrate for the first time that ALDH2 genotypes modify the effects of intake of a small amount of alcohol on haemodynamics and heart rate variability in Japanese men.
Inconsistent results have been reported regarding the association of the angiotensin-converting enzyme (ACE) insertion/deletion (I/D) polymorphism and hypertension. Recent studies of population-based samples of three different areas in Japan presented conflicting results regarding this association. We, thus, investigated the relation between the ACE I/D polymorphism and blood pressure (BP), or the frequency of hypertension, respectively, in 706 Japanese male subjects who participated in the health check-up programme of our hospital. The ACE I/D polymorphism was determined by the polymerase chain reaction technique. Of 706 subjects, 203 were found to have hypertension and the other 503 were found to be normotensive. In all subjects, the frequencies of the DD, ID, and II genotypes were 0.123, 0.432, and 0.445, respectively, and the allelic frequency of the D allele was 0.339. In the younger subjects aged o50 years (n ¼ 264), neither systolic nor diastolic BP differed significantly among the genotypes. Conversely, in the older subjects agedX50 years (n ¼ 442), the systolic BP was significantly higher by 5.9 mmHg in the subjects with the ID genotype than those with the II genotype (Po0.01), and the diastolic BP was significantly higher in the subjects with the DD and ID genotypes by 5.1 and 3.3 mmHg, respectively than those with the II genotype (Po0.05 for each), although age, BMI, percentage of smoking habits, drinking habits, or the use of antihypertensive drugs did not differ significantly among the genotypes. In addition, in the older subjects, the hypertensive subjects showed significantly higher frequencies of the DD and ID genotypes and the D allele than the normotensive subjects. These results demonstrated that there was no significant association of the ACE I/D polymorphism with BP or a prevalence of hypertension in younger Japanese men aged o50 years but there was in older Japanese men aged X50 years.
We investigated the effects of smoking cessation or alcohol restriction on metabolic and fibrinolytic variables in Japanese men. In the smoking study, 35 male subjects [32+/-1 (S.E.M.) years] who habitually smoked cigarettes (29+/-3 cigarettes/day) were told either to keep their usual smoking habits for 1 week, or to abstain from cigarette smoking, using a randomized crossover design. In the alcohol study, 33 male subjects (37+/-1 years) who habitually drank alcohol (64+/-6 ml of ethanol/day) were told either to keep their usual drinking habits for 3 weeks, or to reduce alcohol intake by at least up to a half of their usual drinking amount, using a randomized crossover design. In each study, venous blood samples were drawn after a 12-h overnight fast on the last day of each period, and metabolic and fibrinolytic variables were measured. One-week smoking cessation significantly increased serum high-density lipoprotein (HDL) cholesterol levels (P<0.05), and significantly decreased serum lipoprotein (a) levels (P<0.01) and plasma plasminogen activator inhibitor-1 levels (P<0.05). In contrast, 3-week alcohol restriction significantly decreased serum HDL cholesterol levels (P<0.05) and plasma tissue plasminogen activator levels (P<0.05). These results suggest that smoking cessation has substantial and immediate benefits on lipid and fibrinolytic variables in habitual smokers, whereas alcohol restriction increases cardiovascular risks, in some respects, in habitual drinkers.
Controversy exists as to the origin of plasma adrenomedullin (AM). To elucidate the source of plasma AM, we measured two molecular forms of AM, an active form of mature AM (AM-m) and an intermediate inactive form of glycine-extended AM (AM-Gly), by immunoradiometric assay using specific kits in two female patients with pheochromocytoma before and 3 weeks after surgery. We also measured plasma AM-m, AM-Gly, and AM-T (AM-m + AM-Gly) levels, in addition to plasma epinephrine (E) and norepinephrine (NE) levels, in bilateral adrenal veins of one patient. Although plasma E and NE levels decreased markedly after surgery in these patients, changes in plasma AM appeared to be confined to the normal range. There were no obvious differences in plasma AM-T, AM-m, or AM-Gly levels in adrenal veins between healthy tissue and tumor sides. Furthermore, plasma AM-T, AM-m, or AM-Gly levels in adrenal veins were comparable with those in the infrarenal inferior vena cavae (IVC) or the suprarenal IVC. In contrast, plasma E and NE levels increased in the adrenal vein of the healthy side and increased further in the adrenal vein of the tumor side compared with those in the infrarenal IVC. These results suggest that the origin of plasma E and NE is the adrenal gland and that elevated plasma levels of E and NE in pheochromocytoma are due to excessive production of E and NE in the adrenal gland of the tumor side. In contrast, it is suggested that neither plasma AM levels in the adrenal vein of the healthy side nor those of the tumor side contribute to the systemic levels of plasma AM. The present results appear to be consistent with the hypothesis that the source of circulating AM is systemic vasculature.
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