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Pathophysiology of Hypertension - By: Robert Baird, Posted on: 2007-12-07

Pathophysiology of Hypertension

To understand the pathophysiology of primary hypertension, remember that arterial blood pressure is a product of CO and systemic vascular resistance and that CO is a product of heart rate and Sv. Thus, any change in heart rate, CO, SV, or systemic vascular resistance affects blood pressure.

Several theories attempt to explain the onset of primary hypertension in atrisk patients. These theories suggest that primary hypertension develops through a combination of mechanisms, such as:

increased blood volume

inappropriate autoregulation of blood pressure

overstimulation of sympathetic nervous fibers in the heart and blood vessels

water and sodium retention by the kidneys

hormonal malfunction affecting the kidneys and blood vessels.

In the theory of hypertension induced by increased blood volume, CO increases to keep up with the high volume of blood passing through the heart. The autoregulatory mechanism of the arterial system produces vasoconstriction in an attempt to keep tissue perfusion relatively constant. When the blood volume remains elevated, vasoconstriction causes systemic vascular resistance, leading to hypertension.

Inappropriate autoregulation of the cardiovascular system is another possible cause of primary hypertension. Beginning with elevated CO, hypertension develops through a failure of the autoregulatory mechanism. After CO and blood volume decrease, vascular tone doesn't return to normal. The hypertensive state becomes the new baseline for the cardiovascular system, and autoregulation maintains this elevated blood pressure.

Another theory maintains that the sympathetic nervous systems normal physiologic response to stress may become pathologic, resulting in overstimulation of the sympathetic nervous system and increased vasoconstriction. This overstimulation increases CO and systemic vascular resistance.

Baroreceptors monitor arterial blood pressure. When arterial pressure rises, the baroreceptors stimulate a vagal response, decreasing the heart rate and causing vasodilation. Likewise, when arterial pressure falls, this reflex system causes arterial pressure to rise. The reason this system doesn't function properly in hypertensive patients isn't known, but one theory suggests that baroreceptor sensitivity is reset at a higher level as the body becomes accustomed to the increased blood pressure.

Excessive sodium intake may cause primary hypertension in people with an inherited defect in sodium excretion. In response to elevated blood pressure, diuresis decreases in normally functioning kidneys. Pathologic changes can alter the threshold at which the kidneys excrete water and sodium, thereby altering the arterial blood pressure.

The onset of primary hypertension in some patients may result from interference with the sodium-potassium pump that controls the movement of sodium and potassium across the cell membrane. Also, hypertension may result from excess renin production, which stimulates the release of aldosterone, causing sodium and water retention and increased arterial blood pressure.

Primary hypertension may also be caused by a hormone preventing sodium and calcium excretion. Intracellular calcium, which promotes smooth-muscle contraction, causes vasoconstriction, resulting in increased peripheral resistance and elevated blood pressure.

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