The kidneys play a central role in arterial pressure regulation through mechanisms related to sodium and water excretion. It has long been observed that acute increases in arterial pressure cause increased sodium and water excretion. This is termed pressure natriuresis or pressure diuresis. If an experiment is conducted in which arterial pressure is increased by infusing a systemic vasoconstrictor for several days, systemic vascular resistance and arterial pressure initially rise (Figure 1). After a day or two, arterial pressure returns to normal despite the sustained increase in systemic vascular resistance. The fall in arterial pressure is caused by a transient increase in sodium and water excretion that reduces blood volume and restores arterial pressure. When the arterial pressure is normalized, the sodium balance (sodium output/sodium intake) is also normalized, but at a reduced blood volume. If the changes in sodium excretion are plotted versus arterial pressure, a renal function curve (pressure natriuresis curve) is generated (see Figure 1). An increase in arterial pressure, brought about by increased systemic vascular resistance in this example, temporarily shifts the operating point on the renal function curve from A to B as the increased pressure increases sodium and water excretion. Then, as blood volume decreases in response to the na-triuresis and diuresis, the arterial pressure falls back to its original operating point (A). The arterial pressure returns to its normal value because the reduction in blood volume reduces cardiac output through the Frank-Starling mechanism. These changes occur while the elevated systemic vascular resistance is being maintained by infusion of the vasoconstrictor. Therefore, the kidneys, by regulating blood volume, are ultimately responsible for the long-term regulation of arterial pressure.
If renal excretion of sodium and water is reduced either by extrinsic influences (e.g., increased circulating angiotensin II and aldos-terone) or by intrinsic renal disease, then a higher arterial pressure (i.e., hypertension) is required to produce normal sodium and water excretion. This causes a rightward shift in the renal function curve (Figure 2). Therefore, when pressure natriuresis is impaired, a higher arterial pressure is required to maintain normal sodium balance. The higher arterial pressure is brought about by small reductions in sodium excretion (relative to sodium intake) due to impaired renal sodium handling, which over time increases blood volume and arterial pressure. Then, once the arterial pressure increases sufficiently to restore normal sodium excretion (to match the sodium intake), a new operating point is established (Point B in Figure 2).
For more details on conditions that alter pressure natriuresis curves see the following review article: Hall J: The kidney, hypertension, and obesity. Hypertension 2003;41: 625-633.
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Your heart pumps blood throughout your body using a network of tubing called arteries and capillaries which return the blood back to your heart via your veins. Blood pressure is the force of the blood pushing against the walls of your arteries as your heart beats.Learn more...