Understanding of the mechanisms involved in the development of essential hypertension is incomplete. Many studies have demonstrated that sympathetic overactivity is involved in the development of essential hypertension. In addition, hypertensive patients, as a group, are insulin resistant. The relationship of increased sympathetic activity to insulin resistance in essential hypertension has not been adequately explained. Hypertensive subjects have been reported to have rapid gastric emptying compared to control subjects. They also have increased postprandial hypotensive responses to high carbohydrate meals compared with non-hypertensive control subjects. The author hypothesizes that essential hypertension is the result of a metabolic disregulation in which the body's glucose regulatory system splits into two separate glucose control systems with two different homeostatic set points for fasting and postprandial glucose levels. It is proposed that insulin is the principle regulator of the lower glucose set point while counter-regulatory hormones, predominantly catecholamines, as well as the rate of gastric emptying, are regulators of the upper glucose set point. The tension between these two opposing control systems results in increased sympathetic activity, increased fasting and postprandial glucose and insulin levels and an increased rate of gastric emptying in hypertension. It is hypothesized that increased sympathetic activity from these opposing regulatory systems initiates a vicious cycle that eventually leads to the development of essential hypertension. This hypothesis explains the beneficial effects of agents that either slow carbohydrate absorption or delay gastric emptying on essential hypertension and postprandial hypotension. New therapeutic strategies for treatment of hypertension are suggested by this hypothesis.
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