Factors that cause high blood pressure due to diabetes:
In type 2 diabetes, the mechanism of hypertension is related to sodium retention and increased vascular resistance. If hypertension occurs before diabetes, it is mostly essential hypertension; if hypertension occurs during the course of diabetes, there are 3 possibilities: essential hypertension, systolic hypertension caused by atherosclerosis, Renal hypertension caused by diabetic nephropathy. In type 1 diabetes, hypertension is mostly renal hypertension caused by diabetic nephropathy. Water and sodium retention is the main mechanism, which often occurs immediately after microalbuminuria. The mechanism of diabetes complicated with hypertension is still not fully understood. Hyperglycemia itself inhibits vascular endothelial relaxation, increases intracellular free calcium, and stimulates the transcription of growth factor genes that act on vascular smooth muscle.
Also, the following factors are involved in the pathogenesis of hypertension:1. Hyperinsulinemia
Type 2 diabetes has hyperinsulinemia due to insulin resistance, and type 1 diabetes can also cause hyperinsulinemia due to long-term large amounts of exogenous insulin. Hyperinsulinemia can cause high blood pressure through the following factors:- ① Increase renal sodium and water reabsorption;
- ②Increase the sensitivity of blood pressure to salt intake;
- ③Increase the sensitivity of pressurizing substances and aldosterone to angiotensin Ⅱ;
- ④ Change the electrolyte transport across the membrane, which is manifested by increased intracellular sodium transport, decreased Na-K-ATPase activity, and increased Na-H-ATPase activity;
- ⑤Increase intracellular calcium;
- ⑥ Stimulate the expression of growth factors (especially vascular smooth muscle growth factors);
- ⑦Stimulate sympathetic nerve activity;
- ⑧ Reduce the synthesis of vasodilator prostaglandin;
- ⑨Increase the secretion of endothelin;
- ⑩ Damage to the natriuretic effect of atrial natriuretic peptide.
2. Renin-Angiotensin-Aldosterone System
Due to hyperinsulinemia, recurring water and salt metabolism disorders (such as ketoacidosis), and long-term metabolic control in diabetic patients, the activity of the renin-angiotensin-aldosterone system in the body can be repeatedly increased, which may be related to diabetic patients’ The occurrence of hypertension is related. However, in diabetic patients with nephropathy and azotemia, whether with or without hypertension, the renin-angiotensin-aldosterone system is inhibited, which may be due to water and sodium retention, degeneration of periglomerular cells, and weakened sympathetic nerve activity, And renal prostaglandin deficiency.3. Water and sodium retention
Hyperinsulinemia, increased activity of the renin-angiotensin-aldosterone system, and kidney disease can all lead to water and sodium retention. Water and sodium retention can increase the sensitivity of blood vessels to catecholamines and sympathetic nerves. Studies have shown that even in patients with diabetes and hypertension with stable metabolism and no azotemia, regardless of type 1 or type 2 diabetes, regardless of whether there is retinopathy or diabetic nephropathy, the exchangeable sodium in the body increases by an average of 10%. The blood pressure was significantly positively correlated. After 6 weeks of administration of diuretics to the patient, the sodium exchange can be reduced to normal, and the pressure response of the cardiovascular system to norepinephrine can be restored to normal from an enhanced state. The causes of water and sodium retention also include increased blood growth hormone, decreased serum albumin concentration, decreased colloidal osmotic pressure, and decreased renal vasodilator factors such as prostaglandin E.4. Catecholamines
Hyperinsulinemia, poor blood sugar control (especially when ketoacidosis occurs), the concentration of catecholamines in the body is significantly increased, and sympathetic nerve activity is significantly increased.5. Atherosclerosis and vascular smooth muscle cell proliferation
Diabetes patients often have lipid metabolism disorders, and long-term poor blood sugar control leads to increased glycosylated protein end products (AGEs), which can lead to atherosclerosis. Also, diabetic patients are often accompanied by hyperinsulinemia, and the increased expression of some growth factors (such as transforming growth factor β1, insulin-like growth factor, platelet-derived growth factor, etc.) can lead to vascular smooth muscle hyperplasia. Atherosclerosis and vascular smooth muscle cell proliferation leading to increased peripheral vascular resistance.6. Increased intracellular free calcium
Hyperinsulinemia can lead to an increase in intracellular free calcium. On the other hand, it was found that the free 1,25-(OH)2D3 level in the blood circulation of diabetic patients increased. All of the above can cause an increase in intracellular free calcium, which leads to an increase in arterial vascular resistance. Why does diabetes cause high blood pressure?
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