OBJECTIVE 5: TO UNDERSTAND HOW THESE VARIOUS MECHANISMS ARE INTEGRATED
IN RESPONSE TO SEVERE CHANGES IN BLOOD VOLUME.
A. It is apparent that extracellular fluid volume is regulated by a variety of overlapping mechanisms. Our knowledge regarding the receptors and the mechanisms they activate is fragmentary. Furthermore the role each receptor and each mechanism plays in the various types of ECF volume disturbance is not certain. Nevertheless, it is useful to attempt to piece together the fragments by describing the probable response to severe volume depletion and to acute volume expansion.
Fig. 8-10. The various factors that respond to severe volume depletion and act to reduce the excretion of salt and water.
B. In severe volume depletion, there are two major triggering stimuli: the fall in arterial pressure and the fall in atrial volume (fig. 8-10). These stimuli activate two major systems, the sympathetic nervous system and the juxtaglomerular apparatus. These two systems are interrelated in that the sympathetic nervous system also stimulates the juxtaglomerular apparatus. As a result, the activity of the renin-angiotensin-aldosterone axis is increased. The peritubular capillary pressures are altered so that reabsorption is stimulated. These, and a constellation of other effector mechanisms, reduce the excretion of salt and water. In addition, total peripheral resistance is raised by the sympathetic neural and humoral activity in combination with angiotensin and ADH, so that the effect of the loss of circulating blood volume is minimized. The sympathetic nervous system also decreases venous compliance and increases the pumping activity of the heart.
C. The response to acute expansion of ECF volume begins also with the two major stimuli: The change in atrial volume and the change in arterial pressure (fig. 8-11). The atrial response is probably triggered first as ECF volume rises; the increase in arterial pressure occurs at a higher level of volume expansion. The sympathetic nervous system and the juxtaglomerular apparatus are the two major systems that respond. The atrial secretion of ANF also plays a role. The change in peritubular capillary pressures is probably a major cause of the resulting diuresis.
D. It is much more difficult to try to piece together our information to explain the physiological maintenance of ECF volume in a healthy individual. More research is required. It is important to remember that there are complex interrelationships among these various stimuli, pathways and effectors. None of these factors operate in isolation of the others.
Fig 8-11. The various factors that respond to acute volume expansion and act to increase salt and water excretion.
QUESTIONS:
17. In severe volume depletion what
are the stimuli that trigger the renal response? What major systems are
activated? What alters proximal tubular salt and water reabsorption? What
alters collecting tubular reabsorption?
18. The data listed below were collected in an
experiment on a dog weighing 18 Kg. The ureter of one kidney was
catheterized and slow intravenous infusion of Ringer's solution was
started. After a control clearance period, a large volume of Ringer's
solution was rapidly injected and a continuous infusion begun at a high
rate. 0 30 60
Time
Art. Pres.
Hct
Cin
RPF
V
PNa
UNa
UNaV
FENa
min
mm Hg
%
ml/min
mEq/l
moles/min%
Begin I.V. of Ringer's solution at 1.5 ml/min.
Begin 1st clearance period.
End 1st clearance period.
104
39
27
114
0.47
151
23.8
61
Infuse 600 ml Ringer's solution I.V.
81
Begin infusion of Ringer's solution at 10
ml/min.
110
Begin 2nd clearance period.
125
End 2nd clearance period.
128
33
34
163
1.8
149
98.2
a. Calculate the Na excretion rate and fractional
excretion.
b. What osmotic and volume changes were produced in
each of the three body water compartments by the infusion of the
Ringer's solution?
c. Why did the blood pressure increase?
d. What changes may have occurred in sympathetic
nerve activity? How would this affect the kidney? What changes have
occurred in the signals perceived by the juxtaglomerular apparatus?
e. What factors have contributed to the increase in
Na and H2O excretion?
19. Five subjects, all healthy young males of approximately the same size, abstained from food and drink overnight and then received one of the following treatments:
A. An injection of furosemide.
B. Removal of a liter of blood.
C. Ten additional hours with no fluid intake.
D. One liter of water by mouth in 20 min.
E. I.V. infusion of 2 L. of Ringer's solution in a four-hour period.
The following data were then obtained at the peak of the response to each treatment. The subjects are NOT listed in the order of treatment.
| Art. Pres. | Sodium | U/P | Potassium | Osmolality | V | ||||
| Plasma | Urine | Cr | Plasma | Urine | Plasma | Urine | |||
| mm Hg | mEq/l | mEq/l | mOsmole/kg H2O | ml/min | |||||
| Subject 1: | 120/80 | 141 | 180 | 200 | 4.5 | 122 | 293 | 1220 | 0.6 |
| Subject 2: | 80/60 | 140 | 120 | 225 | 4.4 | 200 | 287 | 1180 | 0.4 |
| Subject 3: | 120/80 | 139 | 13 | 14 | 4.6 | 9 | 282 | 122 | 8.8 |
| Subject 4: | 110/70 | 139 | 110 | 17 | 4.5 | 70 | 287 | 310 | 7.0 |
| Subject 5: | 135/90 | 140 | 135 | 52 | 4.6 | 55 | 287 | 580 | 2.5 |
a. Match the subjects with the treatment.
b. In which subject is the diuresis primarily due
to a low plasma concentration of ADH? Why?
c. In which subject is the stimulus for renin
secretion the greatest? Why?
d. In which subject is the rate of Na excretion the
lowest? Why?
e. Which subject probably has the lowest rate of
aldosterone secretion? Why?
f. In which subject is proximal tubular fluid
reabsorption likely to be depressed because of the pressure changes in
the peritubular capillaries? Why?
g. In which subject is it likely that urine flow
rate is reduced by a combination of depressed GFR and stimulation of
salt and water reabsorption in the proximal tubule? Why?
h. Subject 5 is excreting potassium at about twice
the rate of Subject 1. Why?
i. In which subject is the ability of the medullary
collecting tubules to reabsorb water most impaired by an
impermeability to water? Why? In which subject is it most impaired by
the loss of the countercurrent osmotic gradient?
CIRRHOSIS AND WATER IMMERSION James Crook of Long Acre, had dropsy, jaundice, palsy,
rheumatism, and an inveterate pain in his back. In three immersions, the
swelling of his legs sunk, so did the pain of his back, as did the
jaundice, blowing from his nose a great quantity of bilious yellow matter.
From the rigidity and the pressure of the fluid we may account for his
pissing more than he drank. A. Sutherland: An attempt to ascertain and extend the
virtues of Bath and Bristol Waters (2nd ed.). London: Frederick and
Leaks, 1764. THE EFFECTS OF WATER IMMERSION ...if the blood be thus driven (by the bath) from the
external and internal parts, what becomes of the blood? The heart and
great vessels, it would seem, must be burdened. Such is to a degree the
case; and it is perhaps the stimulus of this fullness and distention or
its action on the elasticity of those great vessels and the heart that
constitutes the reaction (which leads forth the urine in abundant
effusion). Such overloading of the heart and great organs whould be
dangerous in every case if the volume of the blood remained the same. Henry Hartshorne: Water versus hydrotherapy or an
essay on water and its true relations to medicine. Philadelphia: Lloyd
P. Smith Press, 1847.
Treatment A:
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