## Two Determinants of the Long Term Arterial Pressure Level In

Figure 19-3, one can also see that two basic long-term factors determine the long-term arterial pressure level. This can be explained as follows.

Two ways in which the arterial pressure can be increased: A, by shifting the renal output curve in the right-hand direction toward a higher pressure level or B, by increasing the intake level of salt and water.

As long as the two curves representing (1) renal output of salt and water and (2) intake of salt and water remain exactly as they are shown in Figure 19-3, the long-term mean arterial pressure level will always readjust exactly to 100 mm Hg, which is the pressure level depicted by the equilibrium point of this figure. Furthermore, there are only two ways in which the pressure of this equilibrium point can be changed from the 100 mm Hg level. One of these is by shifting the pressure level of the renal output curve for salt and water; and the other is by changing the level of the water and salt intake line. Therefore, expressed simply, the two primary determinants of the long-term arterial pressure level are as follows:

1. The degree of pressure shift of the renal output curve for water and salt

### 2. The level of the water and salt intake line

Operation of these two determinants in the control of arterial pressure is demonstrated in Figure 19-4. In Figure 19-4A, some abnormality of the kidneys has caused the renal output curve to shift 50 mm Hg in the high-pressure direction (to the right). Note that the equilibrium point has also shifted to 50 mm Hg higher than normal. Therefore, one can state that if the renal output curve shifts to a new pressure level, so will the arterial pressure follow to this new pressure level within a few days.

Figure 19-48 shows how a change in the level of salt and water intake also can change the arterial pressure. In this case, the intake level has increased fourfold and the equilibrium point has shifted to a pressure level of 160 mm Hg, 60 mm Hg above the normal level. Conversely, a decrease in the intake level would reduce the arterial pressure.

Thus, it is impossible to change the long-term mean arterial pressure level to a new value without changing one or both of the two basic determinants of long-term arterial pressure—either (1) the level of salt and water intake or (2) the degree of shift of the renal function curve along the pressure axis. However, if either of these is changed, one finds the arterial pressure thereafter to be regulated at a new pressure level, at the pressure level at which the two new curves intersect.

Failure of Increased Total Peripheral Resistance to Elevate the Long-Term Level of Arterial Pressure if Fluid Intake and Renal Function Do Not Change

Now is the chance for the reader to see whether he or she really understands the renal-body fluid mechanism for arterial pressure control. Recalling the basic equation for arterial pressure—arterial pressure equals cardiac output times total peripheral resistance—it is clear that an increase in total peripheral resistance should elevate the arterial pressure. Indeed, when the total peripheral resistance is acutely increased, the arterial pressure does rise immediately. Yet if the kidneys continue to function normally, the acute rise in arterial pressure usually is not maintained. Instead, the arterial pressure returns all the way to normal within a day or so. Why?

The answer to this is the following: Increasing resistance in the blood vessels everywhere else in the body besides in the kidneys does not change the equilibrium point for blood pressure control as dictated by the kidneys (see again Figures 19-3 and 19-4). Instead, the kidneys immediately begin to respond to the high arterial pressure, causing pressure diuresis and pressure natriuresis. Within hours, large amounts of salt and water are lost from the body, and this continues until the arterial pressure returns exactly to the pressure level of the equilibrium point.

As proof of this principle that changes in total peripheral resistance do not affect the long-term level of arterial pressure if function of the kidneys is still normal, carefully study Figure 19-5. This figure shows the approximate cardiac outputs and the arterial pressures in different clinical conditions in which the long-term total peripheral resistance is either much less than or much greater than normal, but kidney excretion of salt and water is normal. Note in all these different clinical conditions that the arterial pressure is also exactly normal.

(A word of caution! Many times when the total peripheral resistance increases, this increases the intrarenal vascular resistance at the same time, which alters the function of the kidney and can cause

Total peripheral resistance (per cent of normal)