American journal of kidney diseases : the official journal of the National Kidney Foundation · 2007
Evaluation of insulin resistance and sodium sensitivity in normotensive offspring of hypertensive individuals.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Pazarloglou Michalis, Spaia Sophia, Pagkalos Emmanouil, Ioannidis Heraklis, Askepidis Nikolaos, Varyemezis Vasilios
Аннотация
BACKGROUND: Sodium sensitivity (SS) and insulin resistance (IR) might be a common link in the pathogenesis of essential hypertension. The aim of the present study is to investigate the relationship, if any, between SS and IR in a population with a family predisposition to develop hypertension.
METHODS: Twenty normotensive subjects aged 20 to 40 years with a family history of hypertension (1 or both parents hypertensive) and no other risk factor (group A) and 10 normotensive subjects aged 20 to 40 years without a family history of hypertension (group B) were enrolled. SS and IR were estimated using the euglycemic clamp technique and correlated in both groups. Blood pressure, mean blood pressure (MAP), and biochemical control were recorded.
RESULTS: The frequency of SS was equal in offspring of hypertensive subjects and the control group. Individuals with a family history of hypertension had a tendency to develop IR (45%) compared with the control group (20%). This group had a greater MAP at both salt-loading and salt-deprivation periods. Increased IR was associated with increased MAP. No significant relationship was found between SS and IR in either the entire sample or the subgroup of individuals with a family history of hypertension. Serum urea and total cholesterol levels were significantly greater in group A. Age, sex, and body mass index were not related to the presence of IR or SS in either group.
CONCLUSION: SS and IR do not relate in young normotensive adults or offspring of hypertensive parents. However, the latter may comprise a high-risk group, currently normotensive, who have an increased possibility to present or develop IR in early adolescent life. Moreover, the increased IR is related to the greater MAP in group A. Thus, they are subject to increased cardiovascular risk because of the subsequent disturbed glucose and lipid metabolism.
METHODS: Twenty normotensive subjects aged 20 to 40 years with a family history of hypertension (1 or both parents hypertensive) and no other risk factor (group A) and 10 normotensive subjects aged 20 to 40 years without a family history of hypertension (group B) were enrolled. SS and IR were estimated using the euglycemic clamp technique and correlated in both groups. Blood pressure, mean blood pressure (MAP), and biochemical control were recorded.
RESULTS: The frequency of SS was equal in offspring of hypertensive subjects and the control group. Individuals with a family history of hypertension had a tendency to develop IR (45%) compared with the control group (20%). This group had a greater MAP at both salt-loading and salt-deprivation periods. Increased IR was associated with increased MAP. No significant relationship was found between SS and IR in either the entire sample or the subgroup of individuals with a family history of hypertension. Serum urea and total cholesterol levels were significantly greater in group A. Age, sex, and body mass index were not related to the presence of IR or SS in either group.
CONCLUSION: SS and IR do not relate in young normotensive adults or offspring of hypertensive parents. However, the latter may comprise a high-risk group, currently normotensive, who have an increased possibility to present or develop IR in early adolescent life. Moreover, the increased IR is related to the greater MAP in group A. Thus, they are subject to increased cardiovascular risk because of the subsequent disturbed glucose and lipid metabolism.