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Vascular dysfunction in monkeys with diet-induced hyperhomocyst(e)inemia

S R Lentz¹, C G Sobey, D J Piegors

¹Department of Internal Medicine, University of Iowa College of Medicine, Iowa City 52242, USA. steven-lentz@uiowa.edu

The Journal of Clinical Investigation

|July 1, 1996

Summary

Elevated homocysteine levels in monkeys led to impaired blood vessel function and reduced anticoagulant properties. This study links moderate hyperhomocysteinemia to vascular dysfunction, highlighting potential risks for vascular disease complications.

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Area of Science:

Cardiovascular Science
Metabolic Disease Research
Vascular Biology

Background:

Elevated plasma homocysteine is a potential risk factor for vascular disease complications.
While in vitro studies show homocysteine affects endothelial cells, in vivo effects on vascular function remain less understood.

Purpose of the Study:

To investigate the association between diet-induced moderate hyperhomocysteinemia and vascular dysfunction in cynomolgus monkeys.

Main Methods:

Induction of moderate hyperhomocysteinemia through a modified diet in cynomolgus monkeys.
In vivo assessment of vasomotor responses using quantitative angiography and Doppler blood flow velocity measurements.
Ex vivo evaluation of carotid artery relaxation and aortic thrombomodulin anticoagulant activity.

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Main Results:

Hyperhomocysteinemic monkeys exhibited significantly reduced leg blood flow post-collagen infusion compared to controls (42% vs. 14% decrease).
Impaired vasodilator responses to acetylcholine and adenosine diphosphate (ADP) were observed in resistance vessels of hyperhomocysteinemic monkeys.
Reduced ex vivo relaxation to acetylcholine and nitroprusside in carotid arteries, alongside a 34% decrease in aortic thrombomodulin anticoagulant activity.

Conclusions:

Diet-induced moderate hyperhomocysteinemia is associated with significant vascular dysfunction in vivo.
Findings suggest impaired endothelial-dependent vasodilation and reduced anticoagulant properties contribute to vascular dysfunction in hyperhomocysteinemia.