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This study found that supraphysiological doses of testosterone alter endothelial relaxation pathways in hypertensive rats, with varied contributions from nitric oxide, prostanoids, and endothelium-derived hyperpolarizing factors, influenced by estrogen and dihydrotestosterone levels.

This study in diabetic db/db mice found that treatment with the antihypertensive agents minoxidil or nebivolol stimulated elastogenesis and inhibited elastolysis, leading to restored elastic fibers, reduced aortic stiffening, and normalized blood pressure.

This study observed that mice with a whole-body deficiency of Cystathionine-β-synthase developed severe hyperhomocysteinemia and related mild symptoms without increased mortality, indicating HHCy may not directly cause end organ damage.

This study observed that in spontaneously hypertensive rats, testosterone's effects on endothelium-dependent vasodilation involved reduced nitric oxide levels, increased oxidative stress, and greater reliance on endothelium-dependent hyperpolarization, with variations in these responses noted when testosterone was combined with either anastrozole or finasteride.

This research found that escin, when applied topically, enhances blood flow in human skin and promotes changes in endothelial cell signaling pathways, suggesting potential benefits for improving cutaneous microcirculation.