Flashcards in Renal Chapter 7: Control of Na/Water Excretion: Regulation of Plasma Volume Deck (80)
What receptors initiate reflexes controlling ADH secretion? Why?
Where are they located?
under conditions of gain/loss of water without solute, osmoreceptors initiate reflexes that control ADH secretion
most osmoreceptors are located in tissues surrounding the 3rd cerebral ventricle
Describe osmoreceptors. What do they signal? How?
in tissues surrounding the 3rd cerebral ventricle
these tissues contain fenestrated capillaries, which allow rapid adjustment of interstitial composition when plasma composition changes
Via these connections, an increase in osmolality stimulates them and increases their rate of ADH secretion
What happens when a person drinks 1L of water?
excess water lowers body fluid osmolality which reflexively inhibits ADH secretion via hypothalamic osmoreceptors.
so water permeability of collecting ducts becomes very low, little or no water is reabsorbed from these segments and a large volume of extremely dilute urine is excreted
What happens when baroreceptor and osmoreceptor inputs oppose each other (eg,
if plasma volume and osmolality are both decreased)?
In general, because of the
high sensitivity of the osmoreceptors, the osmoreceptor influence predominates
over that of the baroreceptor when changes in osmolality and plasma volume are
small to moderate.
However, a very large change in plasma volume will take precedence
over decreased body fluid osmolality in influencing ADH secretion; under
such conditions, water is retained in excess of solute, and the body fluids become
hypo-osmotic (for the same reason, plasma sodium concentration decreases
What happens in diabetes insipidus?
Diabetes insipidus is characterized by a constant water diuresis, as
much as 25 L/day. In most cases, people with diabetes insipidus have lost the
ability to produce ADH because of damage to the hypothalamus or have lost the ability to respond to ADH because of defects in principal cell ADH receptors.
Thus, collecting-duct permeability to water is low and unchanging regardless of extracellular osmolality or volume.
Where are the centers that mediate thirst located?
stimulated both by reduced plasma volume and by increased body fluid osmolality (same factors that stimulate ADH prod.)
angiotensin II can stimulate thirst by direct effect on brain
Draw a flow chart summarizing the major factors that increase tubular sodium and water reabsorption in severe sweating.
Figure 7-17 p 143
Describe inappropriate signaling to kidneys in congestive heart failure and result.
high levels of renin, angiotensin II, aldosterone, catecholamines, and other
mediators. Fluid volume is increased, leading to edema in the lungs, peripheral tissues, or both, which is why this is called congestive heart failure. Because of the high fluid volume, atrial pressures sensed by the cardiopulmonary baroreceptors are high. The high atrial pressures should lead to decreased ADH secretion and decreased sympathetic drive to the kidneys. Instead, these signals are increased,
and the kidneys operate at a new setpoint in which normal sodium excretion
only occurs at the expense of an excessive body fluid volume
Another characteristic of congestive heart failure is high levels of natriuretic
peptides. This is an appropriate response to the high atrial pressures and partially counteracts the sodium-retaining signals to the kidneys but does not restore sodium output to a level that would occur in a healthy person
What is therapy for congestive heart failure?
Therapy for congestive heart failure includes
the use of diuretics to reduce the high fluid volume and drugs that inhibit the
generation of angiotensin II (ACE inhibitors) or block the actions of angiotensin
II (angiotensin receptor antagonists). In addition, synthetic natriuretic peptides
are becoming tools to promote diuresis.
How can renal glomerular disease lead to increase in blood pressure?
renal glomerular disease often leads to inappropriate release of renin with subsequent increases in angiotensin II, aldosterone,
collecting-tubule sodium reabsorption, and finally an increase in blood
In a canine experiment, a dog’s filtered load of sodium in an isolated pump-perfused
kidney is found to be 15 mmol/min. (1) How much sodium do you predict
remains in the tubule at the end of the proximal tubule? (2) If its GFR is suddenly increased
by 33%, how much sodium now is left at the end of the proximal tubule?
(1) 5 mmol/min. Approximately two-thirds of filtered sodium is reabsorbed
by the proximal tubule. (2) 6.6 mmol/min. Filtered sodium rises
from 15 to 20 mmol/min. Glomerulotubular balance maintains fractional
sodium reabsorption at approximately two-thirds of the filtered
Normally aldosterone stimulates the reabsorption of approximately 33 g of sodium chloride/day. If a patient loses 100% of adrenal function, will 33 g of sodium chloride be excreted per day indefinitely?
The answer is no. As soon as the person starts to become sodium deficient
as a result of the increased sodium excretion, the usual sodiumretaining
reflexes will be set into motion. They will, of course, be unable
to raise aldosterone secretion, but they will lower GFR and alter the
other factors that influence tubular sodium reabsorption to compensate
at least partially for the decreased aldosterone-dependent sodium
A patient has suffered a severe hemorrhage and the plasma protein concentration
is normal. (Not enough time has elapsed for interstitial fluid to move into the
plasma.) Does this mean that the peritubular-capillary oncotic pressure is also
The answer is no. It will probably be slightly above normal because of
increased filtration fraction (ie, reduction in GFR and an even greater
reduction in renal blood flow secondary to renal arteriolar constriction
mediated by the renal sympathetic nerve and angiotensin II).
If the right renal artery becomes abnormally constricted, what will happen to renin
secretion by the right kidney and the left kidney?
The right kidney will have increased secretion because of decreased renal
perfusion pressure acting via the intrarenal baroreceptor and decreased
flow to the macula densa. This increased secretion will result in elevated
systemic arterial angiotensin II and elevated arterial blood pressure,
both of which will inhibit renin secretion from the left kidney.
A patient is suffering from primary hyperaldosteronism (ie, increased secretion of
aldosterone caused by an aldosterone-producing adrenal tumor). Is plasma renin concentration higher or lower than normal?
Plasma renin concentration is lower. The increased aldosterone causes the
body to retain sodium, which reflexively inhibits renin secretion. Thus,
one observes high plasma aldosterone and low plasma renin, a strong
tip-off to the presence of the disease because, in almost all other situations,
renin and aldosterone change in the same direction (because the rennin-
angiotensin system is the major control of aldosterone secretion
An agent that increases sodium and water excretion is called a diuretic (even
though natriuretic is probably a better term). Block of sodium reabsorption in the
proximal tubule, loop of Henle, distal tubule, or collecting duct all exert a diuretic
effect. True or false?
The answer is true. Although some diuretic drugs are more potent than
others, blockage at any site results in at least mild diuresis. Because less
than 2% of the filtered load is normally excreted, it does not require a
huge reduction in the percentage reabsorbed to result in a large increase
in the amount of sodium that is excreted
A person is given a drug that dilates both the afferent and efferent arterioles.
Assuming no other action of the drug, what will happen to the percentage of filtered
sodium that this person’s proximal tubule reabsorbs?
It will decrease. This question focuses on the effect of peritubular factors
on proximal sodium reabsorption. Although the GFR will remain
about the same, the renal blood flow increases. The peritubular capillary
pressure will, therefore, rise. At the same time, the peritubular oncotic
pressure will decrease because of the decreased filtration fraction. Both
of these effects tend to reduce fluid reabsorption from the interstitium,
which reduces proximal sodium and water reabsorption.
A new drug is found to have dual actions: It blocks sodium entry pathways in the proximal tubule epithelium, and it binds to ADH receptors in the collecting ducts
and mimics the actions of ADH. Will the final urine contain excess or low amounts of sodium and excess or low amounts of water, and will it be hyperosmotic, isoosmotic,
There will be excess sodium. We cannot be sure of the net effect on water
because there are opposing influences: the excess sodium leading to
increased water excretion and the ADH-like effect leading to decreased
water excretion. The osmolality, for sure, will be hyperosmotic.
Another new drug also has dual actions, this time blocking sodium entry pathways
in the thick ascending limb and exerting ADH-like actions as in Question 7–8.
Now will the final urine contain excess or low amounts of sodium and excess or low
amounts of water, and will it be hyperosmotic, iso-osmotic, or hypo-osmotic?
There will be excess sodium, excess water, and an iso-osmotic urine.
Blocking sodium reabsorption in the thick ascending limb is what
“loop diuretics” do. Not only do they lead to excess sodium and water
in the urine, but they prevent the kidneys from generating a medullary
osmotic gradient. Even with the ADH-like actions of the drug,
the urine cannot become more concentrated than the now iso-osmotic