Related Experiment Videos
Endothelial function and adrenergic reactivity in human type-II diabetic resistance arteries
M J Cipolla1, C T Harker, J M Porter
1Department of Surgery, Oregon Health Sciences University, Portland 97201, USA.
Journal of Vascular Surgery
|May 1, 1996
Summary
Diabetic arteries show increased sensitivity to norepinephrine due to impaired endothelial function. This suggests altered receptor-level mechanisms in type II diabetes, impacting vascular reactivity.
Area of Science:
- Cardiovascular Physiology
- Endocrinology
- Vascular Biology
Background:
- Type II diabetes is associated with vascular dysfunction.
- The role of the vascular endothelium in modulating arterial responses in diabetes requires further investigation.
Purpose of the Study:
- To investigate the endothelial role in modulating adrenergic vasoconstriction in subcutaneous arteries from type II diabetic patients.
- To compare arterial reactivity in diabetic and control subjects.
Main Methods:
- Small subcutaneous arteries from control (n=22) and diabetic (n=18) patients were analyzed using an arteriograph.
- Vascular sensitivity to norepinephrine was assessed in intact, endothelium-denuded, and nitric oxide-inhibited (N omega-nitro-L-arginine) arteries.
- Nitric oxide release and smooth muscle cell responses were also evaluated.
Main Results:
- Diabetic arteries exhibited augmented sensitivity to norepinephrine (lower EC50) compared to control arteries.
- Endothelial removal or nitric oxide inhibition increased norepinephrine sensitivity in control arteries but not in diabetic arteries.
- Stimulated nitric oxide release by acetylcholine was higher in diabetic arteries, while smooth muscle sensitivity to sodium nitroprusside was similar.
Conclusions:
- The endothelium normally mitigates adrenergic reactivity, a function lacking in diabetic arteries, leading to enhanced norepinephrine responsiveness.
- Increased acetylcholine sensitivity in diabetic arteries suggests potential receptor-level alterations.