Hypertension and insulin resistance: role of sympathetic nervous system activity
| Autor: | Richard N. Bergman, F. J. Ortiz-Alonso, Linda Morrow, Mark A. Supiano, Robert V. Hogikyan, William H. Herman, Jeffrey B. Halter |
|---|---|
| Rok vydání: | 1992 |
| Předmět: |
Adult
medicine.medical_specialty Sympathetic nervous system Aging Sympathetic Nervous System Physiology Endocrinology Diabetes and Metabolism medicine.medical_treatment Blood Pressure Guanidines Norepinephrine Insulin resistance Physiology (medical) Internal medicine Medicine Humans Insulin Aged Glucose tolerance test medicine.diagnostic_test business.industry Fasting Glucose Tolerance Test Middle Aged medicine.disease Endocrinology Blood pressure medicine.anatomical_structure Peripheral nervous system Hypertension Catecholamine Regression Analysis Insulin Resistance business medicine.drug |
| Zdroj: | The American journal of physiology. 263(5 Pt 1) |
| ISSN: | 0002-9513 |
| Popis: | he purpose of this study was to test the hypothesis that heightened sympathetic nervous system (SNS) activity contributes to the mechanism by which hypertension is associated with insulin resistance in humans. We performed frequently sampled intravenous glucose tolerance tests to determine tissue sensitivity to metabolic effects of insulin (SI) and measured plasma norepinephrine (NE) levels in 21 normotensive and 14 hypertensive Caucasian subjects. Compared with the normotensive subjects, hypertensive subjects had decreased SI (5.4 +/- 0.5 vs. 4.0 +/- 0.7 x 10(-5) x min-1 x pM-1; P = 0.03) but similar plasma NE levels (normotensive: 1.82 +/- 0.12 vs. hypertensive: 1.73 +/- 0.16 nM; P = 0.23). In a multiple regression model, only body mass index (BMI) and mean arterial blood pressure (MABP) were significant independent predictors of SI [SI = (-0.513)(BMI) + (-0.058)(MABP) + 23.6; r = 0.748; P = 0.0001]; age, plasma glucose, epinephrine, and NE level did not enter this model. As an additional test of this hypothesis, seven hypertensive subjects were restudied after 10 days of guanadrel therapy to determine whether SI would increase during suppression of SNS activity by guanadrel. Despite a significant reduction in plasma NE levels with guanadrel (baseline: 1.63 +/- 0.18 vs. guanadrel: 0.99 +/- 0.14 nM; P = 0.01), there was no significant change in SI (baseline: 2.97 +/- 0.78 vs. guanadrel: 2.41 +/- 0.54 x 10(-5).min-1 x pM-1; analysis of variance P = 0.57). We conclude that, in the Caucasian population we studied, heightened SNS activity is not essential for the insulin resistance observed in hypertensive humans. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|