The prevalence of hypertension reaches up to 67% after 30 years of diabetes duration in type 1 and more than 60% in type 2 diabetes. The mechanisms of increased blood pressure (BP) in type 2 diabetic patients involve several factors mostly related to obesity.
Cardio-vascular vago-sympathetic balance is early impaired in diabetes history, leading to a defect in vagal activity and an excess in sympathetic activity. This profile is associated with prevalent and incident hypertension and the non-dipping nocturnal BP profile. It contributes to peripheral vasoconstriction and artery stiffness, the increase in renin–angiotensin–aldosterone system activity and sodium renal reabsorption. Sympathetic activity is further enhanced in the patients with obstructive sleep apnea syndrome, due to exposure to sleep fragmentation and intermittent hypoxia.
Endothelial dysfunction occurs early in diabetes as a result of several clustered risk factors and oxidative stress. It may alter vasomotion and promote vasoconstrictive tone.
Insulin resistance affects the vessels, accounting for the reduction of vasodilative effect of insulin while hyperinsulinemia may enhance sympathetic activity and depress vagal activity.
The changes in adipokines secretion and effects may also be involved in hypertension. Hyperleptinemia (like hyperinsulinemia) may enhance sympathetic activity while its vasodilative effect is reduced due to leptin resistance and endothelium dysfunction.
GLP-1 may also increase sympathetic activity but improves endothelium function. The role of endogenous GLP-1 in BP regulation needs to be clarified in diabetes.
Finally, hyperglycemia and glucose variability might play a role in hypertension, particularly through changes in peripheral microcirculation.