Vascular Dysfunction in Diabetes and Glaucoma
Vascular Dysfunction in Diabetes and Glaucoma
Endothelial function and its effect on autoregulation have garnered much attention in recent vascular disease research. Several studies suggest vascular autoregulation in retinal, choroidal, and retrobulbar circulation may be compromised in patients with glaucoma. Similarly, substantial evidence indicates that endothelial dysfunction is closely associated with the development of angiopathy in both type 1 and type 2 diabetes. Diabetes may further predispose patients with glaucoma to vascular autoregulatory dysfunction and impairment of these endothelial factors may be amplified in such patients with diabetes.
Furthermore, although studies have shown that atherosclerosis is accelerated in diabetes, little has been done to elucidate its relationship with glaucoma. As numerous endothelial factors protect the blood vessel and discourage atherogenesis, it has been suggested that the initiation of atherosclerosis may be closely related to endothelial dysfunction as well.
The endothelium, which synthesizes and releases relaxing and contracting factors in vessels such as nitric oxide (NO) and endothelin-1(ET-1), undertakes a critical role in vascular homeostasis. NO regulates ocular blood flow and appears to protect cells against pathogenic factors associated with glaucoma and diabetes. Impaired production of NO is a potential pathogenic factor of OAG, and it has even been proposed that increased synthesis and release of NO may eliminate further progression of functional and histologic abnormalities associated with glaucoma. In progressing stages of diabetic retinopathy, serum levels of NO have been shown to increase, which may lead to further vascular dilation, decreased resistance, and increased retinal flow. Although the exact pathophysiological pathways remain puzzling, elevated ET-1 in ocular circulation has also been considered a potential contributor in developing glaucoma. In fact, a recent study found a significant correlation between IOP and concentration of ET-1 levels in the aqueous humor of POAG patients but did not detect any differences in plasma ET-1 levels, suggesting that endothelial factors may influence more than just vasculature. Interestingly, increased levels of ET-1 have also been found in patients with type I and II diabetes and diabetic retinopathy.
Vascular Autoregulation
Endothelial function and its effect on autoregulation have garnered much attention in recent vascular disease research. Several studies suggest vascular autoregulation in retinal, choroidal, and retrobulbar circulation may be compromised in patients with glaucoma. Similarly, substantial evidence indicates that endothelial dysfunction is closely associated with the development of angiopathy in both type 1 and type 2 diabetes. Diabetes may further predispose patients with glaucoma to vascular autoregulatory dysfunction and impairment of these endothelial factors may be amplified in such patients with diabetes.
Furthermore, although studies have shown that atherosclerosis is accelerated in diabetes, little has been done to elucidate its relationship with glaucoma. As numerous endothelial factors protect the blood vessel and discourage atherogenesis, it has been suggested that the initiation of atherosclerosis may be closely related to endothelial dysfunction as well.
The endothelium, which synthesizes and releases relaxing and contracting factors in vessels such as nitric oxide (NO) and endothelin-1(ET-1), undertakes a critical role in vascular homeostasis. NO regulates ocular blood flow and appears to protect cells against pathogenic factors associated with glaucoma and diabetes. Impaired production of NO is a potential pathogenic factor of OAG, and it has even been proposed that increased synthesis and release of NO may eliminate further progression of functional and histologic abnormalities associated with glaucoma. In progressing stages of diabetic retinopathy, serum levels of NO have been shown to increase, which may lead to further vascular dilation, decreased resistance, and increased retinal flow. Although the exact pathophysiological pathways remain puzzling, elevated ET-1 in ocular circulation has also been considered a potential contributor in developing glaucoma. In fact, a recent study found a significant correlation between IOP and concentration of ET-1 levels in the aqueous humor of POAG patients but did not detect any differences in plasma ET-1 levels, suggesting that endothelial factors may influence more than just vasculature. Interestingly, increased levels of ET-1 have also been found in patients with type I and II diabetes and diabetic retinopathy.
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