Aim: 

The present study was designed to examine alterations to the vasodilator and vasoconstrictor reactivity of femoral arteries from adult obese Zucker rats, as a model for the metabolic syndrome, in an attempt to more clearly characterize the vascular dysfunction associated with obesity and insulin resistance.

Methods: 

Seventeen-week-old lean Zucker rats and obese Zucker rats were used for all experiments. Femoral artery was cut into ring segments and they were mounted in a multimyograph for isometric force recording. Cumulative concentration-responses curves to exogenous acetylcholine, nitric oxide donor, noradrenaline and serotonin were obtained.

Results: 

Endothelium-dependent acetylcholine-induced relaxation was reduced in arteries from obese compared to lean Zucker rats. Exogenous NO, added as acidified nitrite, induced an endotelium-independent relaxation comparable in the two groups. Specificity of constrictor reactivity changes was assesed by determining reactivity to potassium chloride, noradrenaline and serotonin. Reactivity to depolarization with potassium chloride was similar in femoral arteries from lean and obese Zucker rats. The sensitivity to noradrenaline and serotonin was significantly increased in femoral arteries from obese compared to lean Zucker rats.

Conclusion: 

The present study provides evidence that metabolic dysfunction induces impairments of endothelial-dependent relaxation whereas responses to the endothelium-independent NO donor were not altered. In addition, the enhanced vasoconstrictor reactivity in femoral arteries from obese animals compared to responses from lean Zucker rats suggests that these functional changes may contribute to the vascular dysfunction.

This study has been supported by grant from Ministerio de Educación y Ciencia SAF2006-09191, Spain.