The Role of Norepinephrine and Insulin Resistance in an Early Stage of Hypertension
The interrelationship between activity of sympathetic nervous system and metabolic risk factors in youth with hypertension (HT) has been poorly studied. The aim of our present study was to assess the interrelationship between metabolic risk factors, such as insulin resistance, concentration of plasm...
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Veröffentlicht in: | Annals of the New York Academy of Sciences 2008-12, Vol.1148 (1), p.490-494 |
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Sprache: | eng |
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Zusammenfassung: | The interrelationship between activity of sympathetic nervous system and metabolic risk factors in youth with hypertension (HT) has been poorly studied. The aim of our present study was to assess the interrelationship between metabolic risk factors, such as insulin resistance, concentration of plasminogen activator inhibitor (PAI)‐1, and catecholamines in an early stage of HT onset. An oral glucose tolerance test was performed in 17 young males with early‐diagnosed nontreated HT grade 1 and 16 gender‐, age‐, and BMI‐matched normotensive controls. Concentrations of glucose, insulin, epinephrine, norepinephrine, PAI‐1, and plasma renin activity (PRA) were determined in venous plasma. Insulin sensitivity indices (ISIs) proposed by Cederholm, Matsuda, and Gutt were calculated. HT had higher baseline levels of norepinephrine, insulin (P= 0.02), and PAI‐1 (P= 0.04). ISIs were lower in HT subjects (P < 0.001). Baseline concentrations of epinephrine were negatively associated with HDL cholesterol (r=−0.415, P= 0.02), ISI Matsuda (r=−0.361, P= 0.04), ISI Cederholm (r=−0.354, P= 0.04), and ISI Gutt (r=−0.429, P= 0.01), and positively with PRA (r= 0.609, P < 0.0001). Positive association was found between baseline concentrations of norepinephrine and PAI‐1 (r= 0.418, P= 0.02). The sympathetic overactivity, which occurs in the early stage of HT may contribute to reduced insulin sensitivity even in young patients and intensify the undesirable development of metabolic cardiovascular risk factors and progress of the disease. |
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ISSN: | 0077-8923 1749-6632 1930-6547 |
DOI: | 10.1196/annals.1410.036 |