Diabetes mellitus is a prevalent chronic disease that affects many people in modern societies. In the past few decades, this disease has risen sharply all over the world. Predictions made by experts in the next 20 years show the disease reaching epidemic proportions by the year 2030. This increase in prevalence is partly due to the impact of obesity which is closely associated with type II diabetes.
Both type I and type II diabetes are characterized by a gradual progression towards generation of specific lesions of blood vessels that affect both the small and larger vessels. The microvascular complications of diabetes are manifested by diabetic retinopathy which causes blindness in adults, diabetic renal disease which currently is the main cause of renal transplantation and dialysis and diabetic neuropathy. According to interventional and epidemiological studies, chronic hyperglycemia is the main cause of diabetic tissue damage. There is an increasing body of evidence which suggest that endothelial dysfunction and oxidative stress are the key mediators of the effects of hyperglycemia.
Since hyperglycemia is the main risk factor that contributes in the development of diabetic complications, knowing how to handle it can be a significant step towards arresting diabetic complications. Many nitric oxide reviews have determined it to be a key factor that plays an important part in vascular physiopathology. The production of nitric oxide depends on the activity of nitric oxide synthase enzymes that are present in a number of body cells.
Diabetic Neuropathy
This is a chronic diabetic complication which usually occurs in two major phenotypes; type I diabetes and type II diabetes. As a microvascular complication, diabetic neuropathy affects both the autonomic and somatic peripheral nerves. Many neuropathic patients manifest signs of neurological dysfunction. These signs include decreased temperature, vibration and sensation for pain. Some other patients have experienced freezing, burning, itching and pain.
Nitric Oxide Effects in Diabetes Polyneuropathy
The production of nitric oxide in the peripheral nerves depends on the nitric oxide synthases. Nitric oxide mediates the nitrergic neurotransmission which controls blood flow and local vasomotor tone. The nitrergic nerves release small quantities of nitric oxide which in turn antagonizes the effect of contractile neurotransmitters.
In both types of diabetes, nitric oxide has a low local level, causes nerve ischemia and inhibits vasodilation. This process takes place in two main phases in the type I diabetes. Within the early stages, nitric oxide synthase expression in nitrergic axons declines. Insulin treatment can be able to reverse the process. In the second phase, the neurons lose their nitric oxide synthase content and thereafter suffer apoptotic degenerative changes. These are irreversible. Nitric oxide derived from endothelial nitric oxide synthase is produced in smaller quantities and this causes a tonic vasodilator effect which plays an important role in the maintenance of nerve vascular tonus.
It is presumed that nitric oxide derived from neuronal nitric oxide synthase is able to contribute more to the blood pressure regulation than nitric oxide derived from endothelial nitric oxide synthase.
Analysis of tissues and arteries in type I and type II diabetic patients indicates both increases and decreases in the expression of endothelial nitric oxide synthase. In order to get a full picture of nitric oxide and its involvement in diabetic Polyneuropathy, you should consider the red blood cells because they carry a major deposit for nitric oxide. The red blood cells play a critical role in ensuring the generation and scavenging of nitric oxide is maintained within a normal balance. This determines the local bioavailability of nitric oxide and also influences vasomotor control.
Nitric oxide is therefore important in the regulation of diabetes mellitus. It ensures that blood flows efficiently and the smooth muscle cells relax adequately so as to allow as much blood as possible to flow through the vessels.
Add relief of diabetic neuropathy to the seemingly never-ending list of benefits of nitric oxide supplements.
Both type I and type II diabetes are characterized by a gradual progression towards generation of specific lesions of blood vessels that affect both the small and larger vessels. The microvascular complications of diabetes are manifested by diabetic retinopathy which causes blindness in adults, diabetic renal disease which currently is the main cause of renal transplantation and dialysis and diabetic neuropathy. According to interventional and epidemiological studies, chronic hyperglycemia is the main cause of diabetic tissue damage. There is an increasing body of evidence which suggest that endothelial dysfunction and oxidative stress are the key mediators of the effects of hyperglycemia.
Since hyperglycemia is the main risk factor that contributes in the development of diabetic complications, knowing how to handle it can be a significant step towards arresting diabetic complications. Many nitric oxide reviews have determined it to be a key factor that plays an important part in vascular physiopathology. The production of nitric oxide depends on the activity of nitric oxide synthase enzymes that are present in a number of body cells.
Diabetic Neuropathy
This is a chronic diabetic complication which usually occurs in two major phenotypes; type I diabetes and type II diabetes. As a microvascular complication, diabetic neuropathy affects both the autonomic and somatic peripheral nerves. Many neuropathic patients manifest signs of neurological dysfunction. These signs include decreased temperature, vibration and sensation for pain. Some other patients have experienced freezing, burning, itching and pain.
Nitric Oxide Effects in Diabetes Polyneuropathy
The production of nitric oxide in the peripheral nerves depends on the nitric oxide synthases. Nitric oxide mediates the nitrergic neurotransmission which controls blood flow and local vasomotor tone. The nitrergic nerves release small quantities of nitric oxide which in turn antagonizes the effect of contractile neurotransmitters.
In both types of diabetes, nitric oxide has a low local level, causes nerve ischemia and inhibits vasodilation. This process takes place in two main phases in the type I diabetes. Within the early stages, nitric oxide synthase expression in nitrergic axons declines. Insulin treatment can be able to reverse the process. In the second phase, the neurons lose their nitric oxide synthase content and thereafter suffer apoptotic degenerative changes. These are irreversible. Nitric oxide derived from endothelial nitric oxide synthase is produced in smaller quantities and this causes a tonic vasodilator effect which plays an important role in the maintenance of nerve vascular tonus.
It is presumed that nitric oxide derived from neuronal nitric oxide synthase is able to contribute more to the blood pressure regulation than nitric oxide derived from endothelial nitric oxide synthase.
Analysis of tissues and arteries in type I and type II diabetic patients indicates both increases and decreases in the expression of endothelial nitric oxide synthase. In order to get a full picture of nitric oxide and its involvement in diabetic Polyneuropathy, you should consider the red blood cells because they carry a major deposit for nitric oxide. The red blood cells play a critical role in ensuring the generation and scavenging of nitric oxide is maintained within a normal balance. This determines the local bioavailability of nitric oxide and also influences vasomotor control.
Nitric oxide is therefore important in the regulation of diabetes mellitus. It ensures that blood flows efficiently and the smooth muscle cells relax adequately so as to allow as much blood as possible to flow through the vessels.
Add relief of diabetic neuropathy to the seemingly never-ending list of benefits of nitric oxide supplements.