The Kidneys and Regulation of Water and Inorganic Ions
511
occurs when blood volume decreases. Therefore, the baro-
receptors transmit fewer impulses via afferent neurons and
ascending pathways to the hypothalamus, and the result is
increased vasopressin secretion. Conversely, increased car-
diovascular pressures cause more fi ring by the baroreceptors,
resulting in a decrease in vasopressin secretion. The mecha-
nism of this inverse relationship is an inhibitory neurotrans-
mitter released by nerves in the afferent pathway.
In addition to its effect on water excretion, vasopres-
sin, like angiotensin II, causes widespread arteriolar constric-
tion. This helps restore arterial blood pressure toward normal
(Chapter 12).
The baroreceptor refl ex for vasopressin, as just described,
has a relatively high threshold—that is, there must be a sizable
reduction in cardiovascular pressures to trigger it. Therefore,
this refl ex, compared to the osmoreceptor refl ex described
next, generally plays a lesser role under most physiological cir-
cumstances, but it can become very important in pathological
states such as hemorrhage.
Osmoreceptor Control of Vasopressin Secretion
We have seen how changes in extracellular volume simultane-
ously elicit refl ex changes in the excretion of
both
sodium and
water. This is adaptive because the situations causing extracel-
lular volume alterations are very often associated with loss or
gain of both sodium and water in proportional amounts. In
contrast, changes in total-body water with no corresponding
change in total-body sodium are compensated for by altering
water excretion
without altering sodium excretion.
A crucial point in understanding how such refl exes are
initiated is realizing that changes in water alone, in contrast
to sodium, have relatively little effect on extracellular volume.
The reason is that water, unlike sodium, distributes through-
out all the body fl uid compartments, with about two-thirds
entering the intracellular compartment rather than simply
staying in the extracellular compartment, as sodium does.
Therefore, cardiovascular pressures and baroreceptors are only
slightly affected by pure water gains or losses. In contrast, the
major effect of water loss or gain out of proportion to sodium
loss or gain is a change in the osmolarity of the body fl
uids.
This is a key point because, under conditions due predomi-
nantly to water gain or loss, the receptors that initiate the
refl exes controlling vasopressin secretion are
osmorecep-
tors
in the hypothalamus. These receptors are responsive to
changes in osmolarity.
As an example, imagine that you drink 2 L of water. The
excess water lowers the body fl uid osmolarity, which results
in an inhibition of vasopressin secretion via the hypothalamic
osmoreceptors (
Figure 14–25
). As a result, the water perme-
ability of the collecting ducts decreases dramatically, water is
not reabsorbed from these segments, and a large volume of
hypoosmotic urine is excreted. In this manner, the excess
water is eliminated.
At the other end of the spectrum, when the osmolarity
of the body fl uids increases because of water deprivation, vaso-
pressin secretion is refl exly increased via the osmoreceptors,
water reabsorption by the collecting ducts increases, and a
very small volume of highly concentrated urine is excreted. By
retaining relatively more water than solute, the kidneys help
reduce the body fl uid osmolarity back toward normal.
To summarize, regulation of body fl uid osmolarity requires
separation of water excretion from sodium excretion. That is, it
requires the kidneys to excrete a urine that, relative to plasma,
either contains more water than sodium and other solutes (water
diuresis) or less water than solute (concentrated urine). This
is made possible by two physiological factors: (1) osmorecep-
tors and (2) vasopressin-dependent water reabsorption without
sodium reabsorption in the collecting ducts.
We have now described two afferent pathways control-
ling the vasopressin-secreting hypothalamic cells, one from
baroreceptors and one from osmoreceptors. To add to the
complexity, the hypothalamic cells receive synaptic input from
many other brain areas, so that vasopressin secretion, and
therefore urine volume and concentration, can be altered by
pain, fear, and a variety of drugs. For example, ethanol inhib-
its vasopressin release, and this may account for the increased
urine volume produced following the ingestion of alcohol,
a urine volume well in excess of the volume of the beverage
consumed.
Figure 14–25
Osmoreceptor pathway that decreases vasopressin secretion and
increases water excretion when excess water is ingested. The opposite
events (an increase in vasopressin secretion) occur when osmolarity
increases, as during water deprivation.
H
2
O excretion
Plasma vasopressin
Collecting ducts
Tubular permeability
to H
2
O
H
2
O reabsorption
Posterior pituitary
Vasopressin secretion
Firing by hypothalamic
osmoreceptors
Body fluid osmolarity
(
H
2
O concentration)
Excess H
2
O ingested
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