Endothelial dysfunction, ADMA and insulin resistance in essential hypertension
Francesco Perticone1, Angela Sciacqua, Raffaele Maio
1Department of Medicina Sperimentale e Clinica G Salvatore, University Magna Graecia of Catanzaro, Italy. perticone@unicz.it
International Journal of Cardiology
|January 27, 2009
Summary
Asymmetric dimethylarginine (ADMA) and insulin resistance (IR) are linked to endothelial dysfunction in hypertension. This study suggests their combined effect may increase cardiovascular risk in hypertensive patients.
Area of Science:
- Cardiovascular Research
- Endocrinology
- Hypertension Research
Background:
- Endothelial dysfunction and insulin resistance (IR) are linked to essential hypertension and cardiovascular risks.
- Asymmetric dimethylarginine (ADMA), a nitric oxide synthase inhibitor, is known to cause endothelial dysfunction.
- The independent or combined roles of ADMA and IR in endothelial dysfunction were previously unexamined.
Purpose of the Study:
- To investigate the relationship between ADMA and IR in hypertensive patients.
- To explore the potential interaction between ADMA and IR in causing endothelial dysfunction.
- To assess endothelial function in relation to ADMA and IR levels.
Main Methods:
- Plasma ADMA levels were measured using high-performance liquid chromatography.
- Insulin resistance was assessed using the homeostasis model assessment (HOMA).
- Endothelial function was evaluated via intra-arterial infusion of acetylcholine and sodium nitroprusside.
Main Results:
- Hypertensive patients exhibited higher ADMA, insulin, HOMA, and C-reactive protein (CRP) levels compared to normotensive controls.
- Acetylcholine-stimulated forearm blood flow (FBF), an indicator of endothelial function, was significantly reduced in hypertensive individuals.
- In hypertensive subjects, HOMA was the primary determinant of FBF (45.5% variation), while ADMA and gender independently determined HOMA (12.3% and 8.3% variation, respectively).
Conclusions:
- The association between ADMA and IR suggests a novel mechanism for ADMA-induced vascular damage in hypertension.
- This interaction may contribute to increased cardiovascular risk in hypertensive patients.
- Further investigation with larger cohorts is recommended to validate these findings.
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