516
Chapter 14
interstitial fl uid of the medulla but a dilution of the
luminal fl
uid.
b. Vasopressin increases the permeability of the cortical
collecting ducts to water, so water is reabsorbed by this
segment until the luminal fl uid is isoosmotic to plasma in
the cortical peritubular capillaries.
c. The luminal fl uid then enters and fl ows through the
medullary collecting ducts, and the concentrated medullary
interstitium causes water to move out of these ducts, made
highly permeable to water by vasopressin. The result is
concentration of the collecting duct fl
uid and the urine.
d. The hairpin-loop structure of the vasa recta prevents the
countercurrent gradient from being washed away.
Renal Sodium Regulation
I. Sodium excretion is the difference between the amount of
sodium fi ltered and the amount reabsorbed.
II. GFR, and hence the fi ltered load of sodium, is controlled
by baroreceptor refl exes. Decreased vascular pressures cause
decreased baroreceptor fi ring and hence increased sympathetic
outfl ow to the renal arterioles, resulting in vasoconstriction
and decreased GFR. These changes are generally relatively
small under most physiological conditions.
III. The major control of tubular sodium reabsorption is the
adrenal cortical hormone aldosterone, which stimulates sodium
reabsorption in the cortical collecting ducts.
IV. The renin-angiotensin system is one of the two major controllers
of aldosterone secretion. When extracellular volume decreases,
renin secretion is stimulated by three inputs: (1) stimulation
of the renal sympathetic nerves to the juxtaglomerular cells by
extrarenal baroreceptor refl exes; (2) pressure decreases sensed
by the juxtaglomerular cells, themselves acting as intrarenal
baroreceptors; and (3) a signal generated by low sodium or
chloride concentration in the lumen of the macula densa.
V. Many other factors infl uence sodium reabsorption. One of
these, atrial natriuretic peptide, is secreted by cells in the atria
in response to atrial distension; it inhibits sodium reabsorption
and it also increases GFR.
VI. Arterial pressure acts locally on the renal tubules to infl uence
sodium reabsorption, an increased pressure causing decreased
reabsorption and hence increased excretion.
Renal Water Regulation
I. Water excretion is the difference between the amount of water
fi ltered and the amount reabsorbed.
II. GFR regulation via the baroreceptor refl exes plays some role
in regulating water excretion, but the major control is via
vasopressin-mediated control of water reabsorption.
III. Vasopressin secretion by the posterior pituitary is controlled
by cardiovascular baroreceptors and by osmoreceptors in the
hypothalamus.
a. A low extracellular volume stimulates vasopressin secretion
via the baroreceptor refl exes, and a high extracellular
volume inhibits it.
b. Via the osmoreceptors, a high body fl
uid osmolarity stimulates
vasopressin secretion, and a low osmolarity inhibits it.
Thirst and Salt Appetite
I. Thirst is stimulated by a variety of inputs, including baro-
receptors, osmoreceptors, and possibly angiotensin II.
II. Salt appetite is not of major regulatory importance in human
beings.
Potassium Regulation
I. A person remains in potassium balance by excreting an amount
of potassium in the urine equal to the amount ingested minus
the amounts lost in feces and sweat.
II. Potassium is freely fi lterable at the renal corpuscle and
undergoes both reabsorption and secretion, the latter
occurring in the cortical collecting ducts and serving as the
major controlled variable determining potassium excretion.
III. When body potassium increases, extracellular potassium
concentration also increases. This increase acts directly on
the cortical collecting ducts to increase potassium
secretion and also stimulates aldosterone secretion. The
increased plasma aldosterone then also stimulates potassium
secretion.
Renal Regulation of Calcium and Phosphate
I. About half of the plasma calcium and phosphate is ionized and
fi l t e r a b l e .
II. Most calcium and phosphate reabsorption occurs in the
proximal tubule.
III. PTH increases calcium absorption in the distal convoluted
tubule and early cortical collecting duct. PTH decreases
phosphate reabsorption in the proximal tubule.
Additional Clinical Examples
I. The most common cause of hyperaldosteronism (too much
aldosterone in the blood) is a noncancerous adrenal tumor
(adenoma) that secretes aldosterone in the absence of
stimulation from angiotensin II. This is sometimes called
Conn’s syndrome.
II. The excess aldosterone causes increased renal sodium
reabsorption and fl uid retention, and is a common cause of
endocrine hypertension.
SECTION B KEY TERMS
aldosterone
507
angiotensin I
508
angiotensin II
508
angiotensin-converting enzyme
(ACE)
508
angiotensinogen
508
antidiuretic hormone
(ADH)
503
aquaporin
502
atrial natriuretic peptide
(ANP)
509
countercurrent multiplier
system
503
diuresis
503
hyperosmotic
503
hypoosmotic
503
insensible water loss
500
intrarenal baroreceptors
508
isoosmotic
503
obligatory water loss
503
osmoreceptor
511
osmotic diuresis
503
pressure natriuresis
510
renin
508
renin-angiotensin system
508
salt appetite
512
vasopressin
503
water diuresis
503
SECTION B CLINICAL TERMS
adenoma
515
arrhythmia
513
central diabetes insipidus
503
diabetes insipidus
503
hyperaldosteronism
515
hyperkalemia
513
hypokalemia
513
nephrogenic diabetes
insipidus
503
primary aldosteronism
(Conn’s syndrome)
515
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