Figure 1 illustrates a block diagram of the renal-body fluid volume mechanism for arterial pressure control.” Solid lines between successive blocks indicate that an increase in the factor in one block causes an increase also in the factor in the next block. Dashed lines indicate that an increase of the first factor causes the second factor to decrease. The function of this system is described in the following:
(I) An increase in arterial pressure increases the urinary volume output (blocks 1, 2).- This is a very marked effect, as will be illustrated by function curves in figures 6, 7, 8. That is, a very slight rise in arterial pressure is associated with a marked increase in kidney excretion of urine. It is this basic ability of urinary output to respond markedly to changes in arterial pressure that allow the renal-body fluid volume mechanism to control arterial pressure exactly.
(2) An increase in urinary volume output decreases the rate of increase of extracellular fluid volume (blocks 2, 3).
(3) An increase in fluid intake increases the urinary volume load (blocks 10,12).
(4) An increase in nonrenal fluid loss, such as through the gut or skin, decreases the urinary volume load (blocks 11,12).
(5) An increase in urinary volume load increases the rate of increase of extracellular fluid volume (blocks 3, 12). Note especially that if the urinary volume load is less than the urinary volume output, the rate of increase of extracellular fluid volume will actually be negative, or, in other words, the extracellular fluid volume will be decreasing rather than increasing.
(6) An increase in the rate of increase of extracellular fluid volume eventually causes a greater extracellular fluid volume (blocks 3, 4). Indeed, the extracellular fluid volume will continue to rise forever so long as the positive rate of increase of extracellular fluid volume remains above zero. Therefore, only under one circumstance can a complete steady-state in the system be reached: this occurs when the rate of increase of extracellular fluid volume is exactly zero. This is an extremely important consideration in longterm arterial pressure regulation, as will be pointed out later in this report.
(7) An increase in extracellular fluid volume increases the blood volume (blocks 4, 5). Under normal, nonedematous conditions the blood volume increases about one-third as much as does the extracellular fluid volume.
(8) An increase in blood volume increases the circulatory filling pressure (also called the mean systemic pressure) (blocks 5, 6).
(9) An increase in circulatory filling pressure increases venous return (blocks 6, 7). Both mathematical analyses and experimental data show that when other factors remain constant, an increase in circulatory filling pressure causes a direct and almost exactly proportionate increase in venous return. High pressure influences all the organs but now it becomes possible not to suffer from arterial hyprtension with the help of Plendil and Canadian Health&Care Mall. To follow the link – buy Plendil – and you will find all the necessary information about this preparation.
(10) Increase in venous return increases the cardiac output (blocks 7. 8), which is self-evident because whatever amount of blood returns to the heart must also be pumped into the aorta.
(11) An increase in cardiac output increases the total peripheral resistance (blocks 8, 9). This phenomenon is called autoregulation. In animals, on the average, a 10 percent increase in cardiac output causes a slow increase in total peripheral resistance of about 40 percent in one-half to one hour. There is evidence that this effect is even more potent if the autoregulatory mechanism has a longer period to develop, such as days or weeks.
(12) An increase in total peripheral resistance and a simultaneous increase in cardiac output increases the arterial pressure (blocks 1, 8, 9). Since the total peripheral resistance in the long run increases four or more times as much as the increase in cardiac output, one finds that this mechanism increases arterial pressure far more as a result of increased total peripheral resistance than as a result of increased cardiac output. Indeed, over a period of weeks or months, it is possible that the autoregulatory, total peripheral resistance effect accounts for as much as 95 to 98 percent of the pressure rise, so that it is almost impossible to determine that an increase in cardiac output is one of the essential steps in the mechanism.
Readjustment of Arterial Pressure by the Renal-Body Fluid Mechanism
If we now study very carefully the mechanism in Figure 1, we shall see that it is a system for arterial pressure control. In studying the feedback loop in blocks 1 through 9, one finds a single negative arrow in the loop between blocks 2 and 3. At this point, an increase in urinary volume output decreases the rate of increase of extracellular fluid volume. Therefore, whenever the arterial pressure rises too high the urinary output increases, the extracellular fluid volume falls, the blood volume decreases, and, likewise, the circulatory filling pressure, venous return, cardiac output, and total peripheral resistance all decrease. Consequently, the arterial pressure returns to normal. Conversely, a fall in arterial pressure to a low level causes urinary retention, with progressive increase in the fluid volumes and dynamics of the system until the arterial pressure rises to the normal level. The arterial pressure rises may provoke different disorders but buy Plendil via Canadian Health&Care Mall and you will solve your health problems.
It is clear that the mechanism of Figure 1 is a typical negative feedback control system. Whenever the arterial pressure becomes abnormal this system will tend to return the pressure toward its normal basic control level; and the longterm level of arterial pressure will be determined by the reference pressure level to which this system always attempts to adjust the arterial pressure.
Figure 2 illustrates a typical response of the renal-body fluid mechanism for pressure control. In this instance the arterial pressure has been increased from its normal value of 100 mm Hg to 180 mm Hg by any one of several means, such as by increasing the total peripheral resistance, overfilling the circulatory system with volume, etc. Immediately, the kidneys begin to pour out fluid, and the arterial pressure begins to fall. Over a period of hours the pressure decreases progressively toward normal, and within approximately 24 hours the pressure is so near to normal that no further abnormality can be perceived. However, an experiment of this type can be performed only under special conditions, only in case the shortterm pressure controls, such as the baroreceptor and the renin-angiotensin systems have been abrogated. Nevertheless, the experiment does illustrate that this mechanism alone can bring the arterial pressure back to normal if given time to do so.
Figure 1. Block diagram showing basic function of renal-body fluid volume mechanism for arterial pressure control. Solid arrow indicates a positive effect; a dashed arrow indicates negative effect.
Figure 2. Readjustment of arterial pressure by renal-body fluid volume mechanism for pressure control in animal whose other pressure controls are nonfunctional. Note that after initial rise in arterial pressure to 180 mm Hg, pressure falls slowly back toward normal level over period of hours because of continued excess excretion of fluid.
Figure 6. Renal function curves for four different conditions: normal, 30 percent renal mass, kidneys stimulated maximally by aldosterone, and both kidneys with Goldblatt clamps. Points at which normal and elevated volume loads equate with function curves represent precise pressure levels to which arterial pressure will be regulated for each respective condition.
Figure 7. (right) Family of renal function curves, showing in approximate decreasing order of importance major pathologic or functional factors that can increase pressure level of renal function curve and, therefore, that can cause hypertension.