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A role for dietary copper in nitric oxide-mediated vasodilation
D A Schuschke1, J T Saari, F N Miller
1Center for Applied Microcirculatory Research, University of Louisville, Kentucky, USA.
Microcirculation (New York, N.Y. : 1994)
|December 1, 1995
Summary
Dietary copper deficiency impairs nitric oxide-mediated arteriolar dilation by inactivating superoxide dismutase, leading to reduced vascular smooth muscle relaxation. Restoring enzyme function with SOD improves dilation.
Area of Science:
- Biochemistry
- Physiology
- Nutritional Science
Background:
- Dietary copper is essential for various enzymatic functions.
- Copper deficiency can impact cardiovascular health.
- Nitric oxide (NO) plays a crucial role in regulating vascular tone.
Purpose of the Study:
- To investigate the effect of dietary copper on nitric oxide-mediated arteriolar dilation.
- To determine the role of copper in the vascular smooth muscle response to vasoactive agents.
Main Methods:
- Male Sprague-Dawley rats were fed copper-adequate or copper-deficient diets for 4 weeks.
- Arteriolar responses to norepinephrine and acetylcholine were measured in cremaster muscle preparations.
- The effect of copper, zinc-superoxide dismutase (SOD) on acetylcholine-induced dilation was assessed.
- Responses to NO-independent vasodilators were also evaluated.
Main Results:
- Copper deficiency did not affect responses to norepinephrine or NO-independent vasodilators (hydrogen peroxide, dibutyryl cGMP/cAMP, papaverine).
- Acetylcholine-induced arteriolar dilation was significantly reduced in copper-deficient rats.
- The impaired dilation in copper-deficient rats was restored by the addition of SOD.
Conclusions:
- Dietary copper restriction inactivates cytosolic copper, zinc-superoxide dismutase (Cu, Zn-SOD).
- This inactivation likely leads to increased superoxide, which inactivates nitric oxide.
- The resulting reduction in nitric oxide bioavailability depresses NO-mediated vascular smooth muscle relaxation.