Hypertension And Diabetes Mellitus
Treatment for diabetes aims to avoid this by keeping blood sugar levels as near to normal as possible. About 25% of people with Type 1 diabetes and 80% of people with Type 2 diabetes have high blood pressure. If you have diabetes and high blood pressure together, this raises your. High blood pressure, or hypertension, is a condition that’s seen in people with type 2 diabetes. If you have high blood pressure, it means that your blood is pumping through your heart and blood vessels with too much force. Having type 2 diabetes and high blood pressure also. Diabetes and high blood pressure are closely related diseases. They occur together so frequently that they are officially considered to be.
Angiotensin II Ang II is to a large degree responsible for triggering vascular inflammation and inducing oxidative stress [ 49 ]. These actions lead to endothelial dysfunction and vascular injury. Gene regulatory network analysis has revealed oxidative stress as a key underlying molecular mechanism in diabetes and hypertension.
The oxidative stress-mediated regulation cascade is the common mechanistic link among the pathogenesis of diabetes, hypertension, and other related inflammatory diseases [ 56 ]. Peroxisome proliferator-activated receptor PPAR activators lower blood pressure, induce favorable effects on the heart, and ameliorate endothelial dysfunction through antioxidant, anti-inflammatory, antiproliferative, antihypertrophic, and antifibrotic effects [ 57 ].
However, recent studies with dual PPAR activators have cast doubts on their clinical efficacy in cardiovascular prevention compared with the original PPAR activators currently marketed [ 5960 ]. Traditional pharmacologic approaches such as statins, ACE inhibitors, and Ang II receptor blockers ARBswhich reduce cardiovascular events in randomized clinical trials, also reduce vascular inflammation in patients with diabetes and hypertension [ 61 — 63 ].
Insulin Resistance Insulin is a pleiotropic hormone that plays a pivotal role in the development of hypertension, diabetes, and the metabolic syndrome. The main metabolic actions of insulin are to stimulate glucose uptake in skeletal muscle and heart and to suppress the production of glucose and very low-density lipoprotein VLDL in the liver [ 66 ].Diabetes and High Blood Pressure: What Can You Eat Food For Diabetic People?
Under fasting conditions, insulin secretion is suppressed, leading to increased glucose synthesis in the liver and kidneys gluconeogenesis and increased conversion of glycogen to glucose in the liver glycogenolysis [ 67 ]. Insulin stimulates the sympathetic nervous system SNS to increase cardiac output and the delivery and utilization of glucose in the peripheral tissues [ 68 ]. Other metabolic effects of insulin include inhibition of glucose release from the liver, inhibition of the release of free fatty acids FFAs from adipose tissue, and stimulation of the process by which amino acids are incorporated into protein [ 67 ].
Insulin resistance, a condition in which defects in the action of insulin are such that normal levels of insulin do not trigger the signal for glucose absorption, denotes an impaired response to insulin in skeletal muscle, liver, adipose, and cardiovascular tissue [ 6768 ]. Insulin resistance arises due to various genetic, acquired, and environmental factors, including obesity [ 69 ].
Diabetes and blood pressure | Diabetes UK
Increased RAAS activities may also cause insulin resistance via the stimulation of Ang II type 1 receptors, which trigger increased production of reactive oxygen species ROS in adipocytes, skeletal muscle, and cardiovascular tissue of obese individuals [ 7071 ]. FFAs are believed to induce insulin resistance and increase the level of oxidative stress [ 707273 ], resulting in endothelial dysfunction and atherogenesis [ 6970 ].
Insulin resistance is associated with impaired insulin signaling, impaired fibrinolysis, and inflammation. Insulin resistance may also result in impaired fibrinolysis, which is characterized by hypercoagulability and elevation of fibrinogen and plasminogen activator inhibitor PAI -1 [ 7677 ]. PAI-1 activity is elevated in a wide variety of insulin resistance patients. Even in patients with normal glucose tolerance, elevated levels of fasting insulin are associated with impaired fibrinolysis [ 76 ].
Therefore, insulin resistance is a prothrombotic state characterized by an elevation of PAI-1 and fibrinogen levels, leading to increased risk of cardiovascular events [ 7577 ]. Insulin resistance may be a result of an overproduction of proinflammatory cytokines eg, IL-6, tumour necrosis factor TNFand CRP and a relative deficiency of anti-inflammatory cytokines eg, adiponectin produced from adipose tissues due to obesity [ 78 ]. Insulin-mediated glucose uptake by muscle varies more than sixfold in apparently healthy individuals [ 79 ], with approximately half of the variability in insulin action being genetically determined and the other half resulting from differences in the degree of adiposity and physical fitness [ 8081 ].
Most patients with type 2 diabetes are insulin resistant, and about half of those with essential hypertension are insulin resistant [ 82 ]. Therefore, insulin resistance is an important common link between diabetes and hypertension. Mental Stress and Sympathetic Nervous System Stressors are intrinsic or extrinsic stimuli leading to disturbances in physiology and psychology, and may threaten health.
Compared with physical stressors, modern stressors arising from psychological threat eg, work stress, domestic violence, and natural disasters are more sustained.
How are diabetes and hypertension linked?
Chronic mental stress, resulting from the modern lifestyle, is frequently associated with physiologic and psychological disturbances, and may indirectly lead to diabetes and hypertension [ 83 — 87 ]. Although epidemiologic investigations have demonstrated that mental stress is associated with hypertension, cardiovascular disease, obesity, and the metabolic syndrome which includes diabetes as a component [ 88 — 92 ], the effect of mental stress on the whole body is not completely understood.
Animal experiments taught us that the mechanisms include renal sympathetic nerve activity RSNA [ 9394 ] and blood pressure control in which baroreflex function [ 95 — 97 ] is involved. In the human body, stimulation of the sympathetic nervous system SNScaused by chronic stress, elevates pulse rate and cardiac minute output and also activates the RAAS, which is another important pressor mechanism [ 86 ].
Increased activity of the SNS also plays a part in the development of impaired glucose [ 87 ] and lipid metabolism [ 8398 ].
- Type 2 Diabetes and High Blood Pressure: What’s the Connection?
- Hypertension and Diabetes Mellitus
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Studying the SNS and RAAS allows us to understand their roles in the etiology and treatment of hypertension, metabolic syndrome, and diabetes [ 84 ]. There is also a link between mental stress and obesity in patients with diabetes and hypertension. A high prevalence of hypertension in obese subjects has been related to psychosocial factors, including chronic stress [ 99 — ].
The hypothalamic—pituitary—adrenal axis was suggested as a key mechanism linking obesity, hypertension, and chronic stress . Therefore, people should reduce stress to escape from the vicious cycle of mental stress, obesity, diabetes, and hypertension. Thus, physical activity reduces the risk of developing diabetes and hypertension. The mechanism involves changes in body weight and glucose tolerance, as well as other factors [ ]. The effect of obesity susceptibility genes on the onset of obesity is influenced by physical activity in the individual.
The former are more likely to carry risk alleles such as rs [ ]. This notion is supported by the observation that there is abnormal glucose metabolism in the offspring of hypertensive parents. There is also a strong association between upregulation of RAAS, hypertension and diabetes.
Further, aldosterone also contributes to hypertension by enhancing SNS activity, decreasing parasympathetic activity, and reducing baroreceptor sensitivity.
Once hypertension is detected both pharmacological and non-pharmacological interventions should be implemented. Instituting lifestyle modifications is paramount, along with medical therapy at the earliest detection of the pre-hypertensive patient. Lifestyle Changes The first objective in any hypertensive diabetic should be to initiate lifestyle changes. These changes should include an improved diet, regular physical activity, weight management and cessation of smoking.
Weight loss has shown to be an effective therapy in hypertension management. Moreover, studies have shown that modest weight loss can lower or even eliminate the need for antihypertensive medication.
The consistent and promising results noted from these studies resulted in initiation of studies to clarify the extent by which the inhibition of RAAS can reduce the incidence of new onset diabetes. Beta-blockers also find their use in diabetes patients with concomitant evidence of coronary artery disease CAD such as anginal symptoms, including anginal equivalents, or post-myocardial infarction MI.
It places an enormous burden on already sparse resources. Diabetes is known to be associated with hypertension. The presence of one increases the risk of having the other. This close relationship between diabetes and hypertension suggests a possible common genetic or pathophysiological process or both.