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Titolo:
Weight gain-induced blood pressure elevation
Autore:
Masuo, K; Mikami, H; Ogihara, T; Tuck, ML;
Indirizzi:
Osaka Univ, Sch Med, Dept Geriatr Med, Suita, Osaka 565, Japan Osaka UnivSuita Osaka Japan 565 ept Geriatr Med, Suita, Osaka 565, Japan Osaka Univ, Sch Med, Dept Community Hlth Nursing, Suita, Osaka 565, Japan Osaka Univ Suita Osaka Japan 565 ty Hlth Nursing, Suita, Osaka 565, Japan Sepulveda VA Med Ctr, Sepulveda, CA USA Sepulveda VA Med Ctr Sepulveda CAUSA veda VA Med Ctr, Sepulveda, CA USA
Titolo Testata:
HYPERTENSION
fascicolo: 5, volume: 35, anno: 2000,
pagine: 1135 - 1140
SICI:
0194-911X(200005)35:5<1135:WGBPE>2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
SYMPATHETIC NEURAL ACTIVATION; INSULIN-RESISTANCE; ESSENTIAL-HYPERTENSION; LEPTIN; HYPERINSULINEMIA; OBESE; HUMANS; YOUNG; VASODILATION; RATS;
Keywords:
obesity; body mass index; hypertension, obesity; investigative techniques; sympathetic nervous system; leptin; insulin;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
30
Recensione:
Indirizzi per estratti:
Indirizzo: Ogihara, T Osaka Univ, Sch Med, Dept Geriatr Med, 2-2 Yamadaoka, Suita, Osaka 565, Japan Osaka Univ 2-2 Yamadaoka Suita Osaka Japan 565 Osaka 565, Japan
Citazione:
K. Masuo et al., "Weight gain-induced blood pressure elevation", HYPERTENSIO, 35(5), 2000, pp. 1135-1140

Abstract

This study was conducted to evaluate the mechanisms in weight gain-inducedblood pressure (BP) elevation focusing, in particular, on the contributions of sympathetic nervous system activity, fasting plasma insulin, and leptin to BP levels. The study design was longitudinal with a cohort of 1897 men. BP, pulse rate, body mass index (BMI), fasting plasma norepinephrine (NE), insulin, and leptin were measured at 6 and 12 months in those 172 lean normotensive, 79 obese normotensive, 64 lean untreated hypertensive, and 38 obese untreated hypertensive men whose BMI increased >10% during the first 6months. At entry, levels of BP, pulse rate, plasma NE, insulin, and leptinin obese subjects, regardless of BP status, were significantly greater than those in lean subjects. The levels of plasma NE, insulin, and leptin increased with weight gain in the 4 study groups. In the subjects with BP elevation, the increase in pulse rate and plasma NE was significantly greater than that in the subjects without BP elevation at both 6 and 12 months for each of the 4 study groups, although the increase in BMI was similar between the subjects with and without BP elevation. In obese but not lean subjects,whether normotensive or hypertensive, the increases in plasma insulin and plasma leptin with weight gain were greater in the subjects with accompanying BP elevation compared with the subjects without BP elevation. On the other hand, at 6 months in lean subjects, the increase in plasma insulin with weight gain in the subjects with BP elevation was actually lower than that in the subjects without BP elevation. These results suggest that weight gain-induced sympathetic overactivity is more tightly linked to weight gain-induced BP elevation than the changes in plasma insulin and leptin that also accompany weight gain. It is probable that sympathetic nervous activation with weight gain is a major mechanism of blood pressure elevation. Hyperinsulinemia and hyperleptinemia may be ancillary factors that contribute to sympathetic nervous stimulation with weight gain.

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Documento generato il 25/11/20 alle ore 18:55:11