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Compensatory hyperinsulinemia and the forearm vasodilator response during an oral glucose‐tolerance test in obese hypertensives

 

作者: Brent Egan,   Konrad Stepniakowski,  

 

期刊: Journal of Hypertension  (OVID Available online 1994)
卷期: Volume 12, issue 9  

页码: 1061-1068

 

ISSN:0263-6352

 

年代: 1994

 

出版商: OVID

 

关键词: Forearm blood flow;obesity;hypertension;insulin resistance;glucose-tolerance test;vascular resistance

 

数据来源: OVID

 

摘要:

ObjectiveTo determine whether obese hypertensive patients manifest a diminished regional vasodilator response to an oral glucose challenge.Methods:Nineteen obese hypertensives (body mass index 34.1±1.3 kg/m2, blood pressure 144±3/96±2 mmHg) and 13 lean controls (23.6±0.3 kg/m2, 127±4/83±3 mmHg) were studied. After 1 week on a standard diet, forearm blood flow (plethysmography), systemic hemodynamics (impedance cardiography), glucose and insulin levels were measured at baseline and again at 15, 30, 60, 90 and 120 min during an oral glucose-tolerance test (OGTT).Results:Forearm blood flow increased after the oral glucose ingestion in obese hypertensives and lean controls. The rise in forearm blood flow was greater in obese hypertensives than in lean controls during the 2-h OGTT. Insulin levels also increased more in obese patients after the glucose load. During the second hour of the OGTT the ratio of changes in forearm blood flow and insulin level, an index of vascular insulin resistance, was similar in both groups. In contrast to the regional hemodynamic findings, total systemic vascular resistance decreased in lean controls but did not change in obese hypertensives during the second hour of the OGTT.Conclusion:The forearm vasodilator response to oral glucose in overweight, non-diabetic hypertensives is not impaired. If dynamic increases in flow are indeed important to insulin-mediated glucose disposal, then these observations raise the possibility that the greater increase of regional blood flow during an OGTT in obese hypertensives represents a component of the compensatory response for their defect in glucose metabolism.

 

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