Common metabolic features of hypertension and type 2 diabetes

Hypertension and type 2 diabetes frequently coexist, suggesting that the two diseases have common pathophysiological bases. This review describes the pathophysiological mechanisms of how type 2 diabetes is frequently associated with hypertension. Multiple common factors mediate between both diseases. Factors that induce both type 2 diabetes and hypertension include obesity-induced hyperinsulinemia, activation of the sympathetic nervous system, chronic inflammation, and changes in adipokines. Vascular complications resulting from type 2 diabetes and hypertension include endothelial dysfunction, vasodilation/constriction dysfunction of peripheral vessels and increased peripheral vascular resistance, arteriosclerosis, and chronic kidney disease. While many of these vascular complications are caused by hypertension, they also exacerbate the pathology of hypertension. In addition, insulin resistance in the vasculature blunts insulin-induced vasodilation and blood flow to skeletal muscle, which contributes to impaired glucose uptake to skeletal muscle and glucose intolerance. In obese and insulin-resistant patients, increase in the circulating fluid volume forms the major pathophysiology of elevated blood pressure. On the other hand, in non-obese and/or insulin-deficient patients, especially those in the middle-or later stages of diabetes, peripheral vascular resistance is the major pathophysiology of hypertension.

Automated summary

Hypertension and type 2 diabetes often occur together due to shared pathophysiological mechanisms. Both diseases are induced by factors such as obesity-induced hyperinsulinemia, activation of the sympathetic nervous system, chronic inflammation, and changes in adipokines. Vascular complications resulting from these diseases include endothelial dysfunction, peripheral vasodilation/constriction dysfunction, arteriosclerosis, and chronic kidney disease. Insulin resistance in the vasculature and increased fluid volume are major factors contributing to elevated blood pressure in obese and insulin-resistant patients, while peripheral vascular resistance plays a major role in hypertension in non-obese and/or insulin-deficient patients.