How does obesity lead to hypertension? An analysis of blood volume and hormone mechanisms.

Hypertension

Hypertension not only significantly increases the incidence of coronary heart disease, but is also a major cause of cerebrovascular accidents and damage to cardiac and renal function. Statistics show that the prevalence of hypertension in obese patients is 2 to 6 times higher than in those of normal weight.

I. Pathogenesis of Hypertension Caused by Obesity

The mechanism by which obesity affects blood pressure is not yet fully understood, but possible mechanisms include:

1. Increased Blood Volume and Cardiac Output
Obese individuals have a significant increase in adipose tissue, which actively participates in metabolic activities. Even at rest, each 100g of adipose tissue requires 2-3ml of blood per minute. Although this is only equivalent to 1/20th of the cerebral blood flow, the large amount of adipose tissue results in a corresponding increase in total blood flow. Obese patients experience increased cardiac output, not through increased heart rate, but through increased stroke volume. Increased blood volume in obese patients means that if peripheral resistance decreases, blood pressure can remain normal; however, if peripheral resistance remains unchanged, blood pressure will rise.

2. Hyperinsulinemia or abnormal renin-aldosterone relationship can cause sodium and water retention. Insulin promotes sodium reabsorption in the distal renal tubules, leading to sodium retention and hypertension, but no change in glomerular filtration rate or aldosterone concentration is observed. Exercise and physical activity can lower plasma insulin and blood pressure, but the decrease in blood pressure is not proportional to the reduction in body fat. A low-calorie diet with unlimited salt can lead to weight loss and lower blood pressure, accompanied by decreased plasma renin activity and aldosterone levels. However, some believe that blood pressure decreases with weight loss without a decrease in plasma renin and aldosterone levels. Low-calorie diets lead to weight loss and lower blood pressure, which is related to decreased sympathetic nerve activity, decreased plasma norepinephrine and epinephrine concentrations, and increased dopamine levels. Restricting carbohydrates can lower plasma norepinephrine and epinephrine concentrations. Obesity can promote the conversion of thyroid hormones to triiodothyronine, which increases the number of β-adrenergic receptors, thereby increasing the sensitivity of blood vessels to pressor mechanisms. Thyroid hormones and catecholamines work synergistically to promote blood pressure elevation. Obese individuals also have active adrenal cortex function, increased cortisol conversion rate, and enhanced hydroxylation of corticosterone and deoxycorticosterone. In summary, although obesity is associated with hypertension, elevated aldosterone, enhanced pressor response, capillary compression, and elevated insulin levels, there is insufficient evidence to support these claims, and the pathogenesis remains unclear. Many obese individuals do not have hypertension, and even those who are extremely obese may have normal blood pressure.