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1 College of Health, University of Utah, Salt Lake City, UT, USA
2 Internal Medicine, University of California, Davis, CA, USA
3 Pharmacology, University of Aarhus, Aarhus, Denmark
* To whom correspondence should be addressed. E-mail: j.david.symons{at}hsc.utah.edu.
Earlier we reported that dietary folate-depletion causes hyperhomocysteinemia (HHcy) and arterial dysfunction in rats. Both HHcy and low-folate (LF) are risk factors for cardiovascular disease. Therefore, the dysfunction we observed could have resulted from HHcy, LF, and/or their combination (HHcy+LF). We tested the hypothesis that HHcy-induced vascular dysfunction is more severe in the presence of LF. Four groups of rats consumed diets for 
10 weeks that produced plasma homocysteine (tHcy, µM) and liver folate (µg folate / g liver) concentrations, respectively, of 7±1 and 15±1 (Control, Con; n=16), 17±2 and 15±2 (HHcy; n=17), 10±1 and 8±1 (LF; n=14), and 21±2 and 8±1 (HHcy+LF; n=18). We observed that maximal acetylcholine (ACh)-evoked vasorelaxation was greatest in aortae and mesenteric arteries from Con rats vs. all groups. While the extent of dysfunction was similar between LF and HHcy animals, it was less severe compared to arteries from HHcy+LF rats. Maximal ACh-evoked vasorelaxation in coronary arteries was not different between Con and LF rats, but both were greater than HHcy+LF animals. In segments of aortae: 1) ACh-evoked vasorelaxation was similar among groups after incubation with the non-enzymatic intracellular O2- scavenger Tiron; 2) vascular O2- estimated using dihydroethidium staining was greatest in HHcy+LF vs. all groups; and 3) tension development in response to nitric oxide synthase inhibition was greatest in Con vs. all other groups. We conclude that HHcy+LF evokes greater dysfunction than either HHcy alone (aortae, mesentery) or LF alone (aortae, mesentery, coronary), likely by producing more O2- within the vasculature and thereby reducing nitric oxide bioavailability.
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