Fluid, Electrolyte, and Acid-Base Balance
Potassium is also part of the body’s buﬀer system, which
resists changes in the pH of body ﬂuids. ShiFs of hydrogen
) into and out of cells induce corresponding shiFs
in the opposite direction to maintain cation balance.
Consequently, EC± potassium levels rise with acidosis, as K
leaves and H
enters the cells, and fall with alkalosis, as K
enters the cells and H
leaves them to enter the EC±. Although
these pH-driven shiFs do not change the total amount of K
in the body, they can seriously interfere with the activity of
neurons and muscle ﬁbers because the relative IC±-EC± po-
tassium concentration directly aﬀects the resting membrane
potential of these cells. K
excess in the EC± decreases their
membrane potential, causing depolarization, oFen followed by
reduced excitability. Too little K
in the EC± causes hyperpo-
larization and nonresponsiveness.
²e heart is particularly sensitive to K
levels. Both too much
and too little K
(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
Atrial natriuretic peptide (ANP)
of the kidney
Mechanisms and consequences of ANP release.
Renin release also inhibits ADH and aldosterone release and hence the effects of those hormones.