Human Physiology, 14th edition (2016)

608 Chapter 17

Relationship Between

Na^1 , K^1 , and H^1

The plasma K^1 concentration indirectly affects the plasma H^1

concentration (pH). Changes in plasma pH likewise affect the

K^1 concentration of the blood. When the extracellular H^1 con-

centration increases, for example, some of the H^1 moves into

cells and causes cellular K^1 to diffuse outward into the extra-

cellular fluid. The plasma concentration of H^1 is thus decreased

while the K^1 increases, helping to reestablish the proper ratio

of these ions in the extracellular fluid. A similar effect occurs in

the cells of the distal region of the nephron.

In the cells of the late distal tubule and cortical collect-

ing duct, positively charged ions (K^1 and H^1 ) are secreted in

response to the negative polarity produced by reabsorption of

Na^1 ( fig. 17.28 ). Acidosis (increased plasma H^1 concentration)

increases the secretion of H^1 and reduces the secretion of K^1

into the filtrate. Acidosis may thus be accompanied by a rise

in blood K^1. By contrast, alkalosis (lowered plasma H^1 con-

centration) increases the renal secretion of K^1 into the filtrate,

and thus the excretion of K^1 in the urine. If, on the other hand,

hyperkalemia is the primary problem, there is an increased

secretion of K^1 and thus a decreased secretion of H^1. Hyperka-

lemia can thus cause an increase in the blood concentration of

H^1 and acidosis.

Because aldosterone promotes the secretion of both K^1

and H^1 into the filtrate, an abnormally high aldosterone secre-

tion (as in primary hyperaldosteronism) causes both hypoka-

lemia and metabolic alkalosis. Conversely, abnormally low

aldosterone secretion (as in Addison’s disease) can produce

hyperkalemia accompanied by metabolic acidosis.

Renal Acid-Base Regulation

The kidneys help regulate the blood pH by excreting H^1 in the

urine (mostly in buffered form, as described shortly) and by

reabsorbing bicarbonate. Because the kidneys normally reab-

sorb almost all of the filtered bicarbonate and excrete H^1 , nor-

mal urine contains little bicarbonate and is slightly acidic (with

a pH range between 5 and 7). The mechanisms involved in the

produced by the atria of the heart and secreted in response to
the stretching of the atrial walls by increased blood volume. In
response to ANP action, the kidneys lower the blood volume
by excreting more of the salt and water filtered out of the blood
by the glomeruli. Atrial natriuretic peptide thus functions as an
endogenous diuretic.

Figure 17.27 Homeostasis of plasma Na^1. This is
the sequence of events by which a low sodium (salt) intake leads
to increased sodium reabsorption by the kidneys. The dashed
arrow and negative sign indicate the completion of the negative
feedback loop.

Stimulus Negative feedback correction

Low plasma

Na+ concentration

Hypothalamus Aldosterone

Na+ reabsorption in

cortical collecting duct

Na+ retention

in blood

Low Na+

intake

Posterior pituitary Adrenal cortex

ADH Angiotensin II

Water reabsorption Renin

in collecting ducts

Urine volume Blood volume Juxtaglomerular apparatus

Sympathetic

nerve activity

Sensor

Integrating

center

Effector

Table 17.6 | Regulation of Renin and Aldosterone Secretion

Stimulus

Effect on Renin

Secretion

Angiotensin II

Production

Aldosterone

Secretion Mechanisms

↓Blood volume Increased Increased Increased Low blood volume stimulates renal baroreceptors; granular

cells release renin.

↑Blood volume Decreased Decreased Decreased Increased blood volume inhibits baroreceptors; increased

Na^1 in distal tubule acts via macula densa to inhibit

release of renin from granular cells.

↑ K^1 None Not changed Increased Direct stimulation of adrenal cortex

↑Sympathetic

nerve activity

Increased Increased Increased a-adrenergic effect stimulates constriction of afferent arterioles;

b-adrenergic effect stimulates renin secretion directly.