Chapter 26
Fluid, Electrolyte, and Acid-Base Balance
1001
26
Potassium is also part of the body’s buffer system, which
resists changes in the pH of body fluids. ShiFs of hydrogen
ions (H
1
) into and out of cells induce corresponding shiFs
of K
1
in the opposite direction to maintain cation balance.
Consequently, EC± potassium levels rise with acidosis, as K
1
leaves and H
1
enters the cells, and fall with alkalosis, as K
1
enters the cells and H
1
leaves them to enter the EC±. Although
these pH-driven shiFs do not change the total amount of K
1
in the body, they can seriously interfere with the activity of
excitable cells.
neurons and muscle fibers because the relative IC±-EC± po-
tassium concentration directly affects the resting membrane
potential of these cells. K
1
excess in the EC± decreases their
membrane potential, causing depolarization, oFen followed by
reduced excitability. Too little K
1
in the EC± causes hyperpo-
larization and nonresponsiveness.
²e heart is particularly sensitive to K
1
levels. Both too much
and too little K
1
(hyperkalemia and hypokalemia, respectively)
can disrupt electrical conduction in the heart, leading to sudden
death (Table 26.1 and p. 684).
Stretch of atria
of heart due to
BP
Atrial natriuretic peptide (ANP)
Adrenal cortex
Hypothalamus and
posterior pituitary
Collecting ducts
of kidneys
JG complex
of the kidney
ADH release
Aldosterone release
Na
+
and H
2
O reabsorption
Blood volume
Vasodilation
Renin release*
Blood pressure
Releases
Negative
feedback
Targets
Effects
Effects
Inhibits
Effects
Inhibits
Results in
Results in
Angiotensin II
Figure 26.9
Mechanisms and consequences of ANP release.
*
Renin release also inhibits ADH and aldosterone release and hence the effects of those hormones.
previous page 1035 Human Anatomy and Physiology (9th ed ) 2012 read online next page 1037 Human Anatomy and Physiology (9th ed ) 2012 read online Home Toggle text on/off