Renal Chapter 7: Control of Na/Water Excretion: Regulation of Plasma Volume Flashcards Preview

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How does GFR represent a mechanism for altering ECF volume?

a change in sodium filtered resulting from a change in GFR is also accompanied by a change in the amount of water filtered.


Describe reflex control of GFR.

Draw flow charts for A) the effects of increased salt and water in ECF and B) increased salt in ECF.

reflex control of GFR is mediated by changing resistance of afferent and efferent arteriolar resistances. Changes in resistance are produced by changes in renal sym. nerve activity and circulating levels of (catecholamines?)

p 125


How does high pressure affect levels of intrarenal angiotensin II in the intermediate response?

How are Na-H exchangers effected?

high pressure reduces a reduction in proximal tubular sodium reabsorption because of a reduction in the number
of functional transporters (Na-H antiporters) in the apical membrane of the proximal tubule epithelial cells. The reduction is probably in response to reduced levels of angiotensin II. There is also an increase (usually small) in glomerular filtration rate (GFR) and
an increase in peritubular hydrostatic pressure and renal interstitial pressure that favor reduced absorption of salt and water in the cortex (particularly from the proximal nephron).
ECF, extracellular fluid

levels of intrarenal angiotensin II.

Number of Na-H exchangers in apical membrane is strongly influenced by angiotensin II, when its levels fall, Na-H exchangers are withdrawn, along with a comcomitant reduction in activity of Na/K ATPase in BL membrane.

result of reduction in angiotensin II in response to high renal artery pressure is less Na absorption, and more presentation of sodium to loop of Henle and therefore more excretion..

See figure 7-10 p 126


What happens if peritubular levels of angiotensin II are kept constant by experimental means?

then pressure natriuresis and diuresis are strongly blunted or even eliminated

A key feature of pressure natriuresis and diuresis is that the degree of salt and
water excretion for a given rise in pressure varies with the volume status of the


Describe how ECF volume affects pressure natriuresis when volume is high/low.

If the ECF volume is normal or high and the renal artery pressure rises, pressure natriuresis
and diuresis are very effective in increasing excretion of sodium and water and reducing blood volume. On the other hand, if ECF volume is low and the renal artery pressure rises, there is much less salt and water loss. It appears that the volume status of the body acts as a gain control on pressure natriuresis and diuresis. There is potent pressure natriuresis and diuresis when ECF volume is high, and much less pressure natriuresis and diuresis when ECF volume is depleted


How/why does a rise in pertitubular capillary pressure affect net reabsorption?

reduces net reabsorption (and therefore causes more excretion)

Starling forces...high capillary pressure opposes reabsorption.


High interstitial pressure should favor reabsorption, so why does it oppose it?

an increased interstitial
pressure causes back-leak of reabsorbed fluid from the interstitial space across the tight junctions into the tubule so pressure doesn't alter cellular transport mechanisms for sodium and water but rather reduces the net reabsorption achieved by these mechanisms (particularly in the "leaky" proximal tubule)

In effect, if the interstitium gets “too full,” then it is difficult to transport more fluid into it. Put another way, high interstitial pressure does more to oppose the movement
of fluid from tubule to interstitium than it does to promote the movement
of fluid from interstitium to capillary


How do changes in GFR cause changes in PPC and piPC?

PPC is set by (1) arterial pressure and (2) the combined vascular resistances of the
afferent and efferent arterioles, which determine how much of the arterial pressure is lost by the time the peritubular capillaries are reached. piPC is set by (1) arterial oncotic pressure and (2) filtration fraction (GFR/RPF), which determine
how much of the oncotic pressure increases from its original arterial value during
passage through the glomeruli.


Fluid loss from the body end with 3 changes that affect GFR. Describe.

lower GFR

increased constriction of aff/eff arterioles (induced by renal nerves and angiotensin II)

decreased arterial hydraulic pressure

increased arterial oncotic pressure

Figure 7–10 illustrates how these same 3 factors also decrease renal interstitial hydraulic pressure and, hence, increase
sodium reabsorption. Thus, homeostatic responses that tend to lower GFR
in response to a reduction in body sodium also usually increase sodium reabsorption,
the “desired” homeostatic event of preserving volume in response to bodily
fluid depletion


What happens with a high salt diet or expansion of the ECF volume?

1) decreased plasma oncotic pressure (resulting from dilution of plasma proteins)

2) increased renal arterial pressure

3) renal vasodilation secondary to decreased activity of the renal sympathetic nerves and decreased angiotensin II

(GFR increases a small amount and so does interstitial pressure which reduces fluid reabsorption)


What is glomerulotubular balance?

in regulation of sodium excretion, control of tubular sodium reabsorption is more important than control of GFR.

(change in GFR automatically induces a proportional change in the reabsorption of sodium by the proximal tubules so that the fraction reabsorbed (but not amount) remains relatively constant.

(change in GFR still reflected as change in sodium and water presented to loop of Henle)

so when fraction reabsorbed is changed, the change is caused by processes other than changes in GFR.


mechanisms responsible for matching changes in tubular reabsorption to
changes in GFR are completely intrarenal (ie, glomerulotubular balance requires
no external neural or hormonal input;


How do autoregulation and glomerulotubular balance work together?

autoregulation prevents GFR from changing too much in direct response to changes in bp

glomerulotubular balance blunts the sodium-excretion response to whatever changes in GFR does occur


Where does independent control (when sodium ingestion and water ingestion both highly variable and unrelated to e/o... one in excess must be excreted more) take place?

most processes for independent control take place in distal nephron


What does aldosterone do and what is the most important physiological factor controlling levels of aldosterone?

aldosterone -sodium retenton (vital in correcting long term changes in bp)

important controlling factor is circulating levels of angiontensin II

circulating angiotensin II will stimulate the adrenal cortex to
produce aldosterone.5 This targets the distal nephron to increase sodium reabsorption
and thus increase total body sodium and blood volume to produce a longterm
correction to total body sodium content and mean blood pressure


Where does aldosterone stimulate sodium reabsorption?

mainly in the cortical connecting tubule and cortical collecting duct, specifically by principal cells.

fine-tuning (90% of sodium reabsorbed by this point)

2% of filtered sodium able to be controlled by aldosterone.


Describe the mechanism of aldosterone's action, receptors etc.

enough lipid character to freely cross principal cell membranes, then combines w receptors in cytoplasm

receptors undergo conformational change that revelas nuclear localization signal. receptor transported to nucleus, acts as a transcription factor that promotes gene expression and synthesis of messenger RNA (mRNA). The mRNA mediates the translation
of specific proteins. The effect of these proteins is to increase the activity or
number of luminal membrane sodium channels and basolateral membrane Na-KATPase
pumps to exactly supply what is needed to promote increased reabsorption
of sodium

figure 7-11 p 131


What factors regulate aldosterone secretion?

angiotensin II
elevated plasma K conc. stimulates aldosterone secretion

atrial natriuretic factors inhibit secretion


Describe prostaglandin activity.

Autoregulation of GFR involves local production of prostaglandins in conditions
when strong vasoconstriction might by itself reduce GFR and renal blood flow too much

intrarenal (autoregulatory) prostaglandin production opposes the actions of angiotensin II on the kidneys... prostaglandin prod. leads to vasodilation of arterioles and relaxation of mesangial cells

Increased local (intrarenal) angiotensin
II concentrations associated with renin release and increased sympathetic
input stimulate the production of prostaglandins.


Draw a flow chart of a drop in blood pressure leading to tubular sodium reabsorption. Label where each even mainly takes place.

P 133


Describe the vasodilatory effect of prostaglandins on angiotensin II and renal arterioles and blood flow and GFR.

vasodilatory effect of prostaglandins dampens the effect of angiotensin II and sympathetic input on renal arterioles and permits a reasonable, but reduced blood flow and GFR to continue


The macula densa cells at the end of the thick ascending limb have Na-K-
2Cl symporters that can avidly take up Na, Cl, and K and cause the cells to swell dramatically when GFR (NaCl delivery) is high. Describe the mechanism.

The increased
Na and Cl in the lumen of the thick ascending limb stimulate the Na-H antiporter
and depolarizes the cells (as in thick ascending limb cells, the K recycles
via K channels). This depolarization leads to Ca entry across the basolateral membrane.
The rise in Ca leads to the release of ATP from the basolateral surface of the cells in close proximity to the glomerular mesangial cells. This ATP stimulates
purinergic P2 receptors on the mesangial cells and afferent arteriolar smooth
muscle cells. P2 receptor stimulation increases Ca in these cells and promotes
contraction. In addition, it is the increased Ca in the afferent arteriolar cells that
reduces renin secretion.

flow chart 7-13 p 134


What is the effect of contraction of mesangial cells?

Contraction of mesangial cells decreases the effective filtration area, which decreases

Contraction of the afferent arteriolar smooth muscle cells increases
afferent resistance and decreases RBF and GFR


Draw a flow chart for the mechanism of tubuloglomerular feedback.

Figure 7-14

p 135


What are natriuretic peptides?
What is the source? Action? Promote what?

In what type of patients may these peptides be elevated?

they promote excretion of sodium in the urine

ANP (atrial)
BNP (brain)

main source of both natriuretic peptides is heart.

vascular and tubular actions- relax afferent arteriole, promoting increased filtration, and act at several sites in tubule. inhibit release of renin, inhibit the actions of angiotensin II that normally promote reabsorption of sodium and act in the medullary collecting duct to inhibit sodium absorption.

greatly elevated in patients w heart failure and serve as diagnostic indicators


Describe the function of ADH. Where does it act? What stimulates its secretion?

major function of ADH is to increase permeability of cortical and medullary collecting ducts to water, therby decreasing excretion of water

in addition, ADH also increases sodium reab. by cortical collecting duct (same seg. influenced by aldosterone)

secretion of ADH (like aldosterone) are stimulated when plasma volume is reduced..they act together


Which of the following hormones increase or decrease sodium reabsorption?

cortisol, parathyroid hormone, progesterone, glucagon, growth hormone, thyroid hormone, insulin

Cortisol, estrogen, growth hormone,
thyroid hormone, and insulin enhance sodium reabsorption,

progesterone, and parathyroid hormone decrease it


What two variables of renal function control sodium excretion?

GFR and rate of sodium reabsorption

rate controlled by:
renin-angiotensin-aldosterone hormonal system, renal sympathetic
nerves, direct effects of arterial blood pressure on the kidneys (pressure natriuresis),
and atrial natriuretic factors

renal interstital hydraulic pressure and several renal paracrine agents


In regards to mechanisms of sodium excretion, distinguish proxmial nephron mechanisms and distal nephron effects

(1) proximal nephron mechanisms (control of GFR, pressure natriuresis, and, to a lesser extent, changes in Starling forces) that lead to coupled changes in sodium and water excretion and

(2) distal nephron effects in which sodium can be reabsorbed independently of water. The proximal mechanisms are primarily involved in excreting excess ECF volume, whereas the distal mechanisms alter sodium excretion when ingestion of
sodium is not balanced by ingestion of water.

Both types of mechanisms can alter blood pressure because of the intimate relationship among total body sodium and
water, blood volume, and blood pressure.


Water excretion conceptually consists of 2 major components. Describe them.

a proximal nephron component, in which water is absorbed along with sodium as an isotonic
fluid, and a distal nephron component, in which water can be reabsorbed independent of sodium.

The proximal nephron component is primarily a mechanism to regulate ECF volume in response to changes in blood pressure,

while the distal nephron rate of water reabsorption is independent of sodium reabsorption. It is determined mainly by ADH, which increases the water permeability of the collecting ducts, thereby increasing water reabsorption and, hence, decreasing water


Describe where ADH is produced and where those cells are located. What are the most important inputs to those cells?

ADH is a peptide produced by a discrete group of hypothalamic neurons whose cell bodies are located in the supraoptic and paraventricular nuclei and whose axons
terminate in the posterior pituitary gland, from which ADH is released into
the blood. The most important of the inputs to these neurons are from cardiovascular
baroreceptors and osmoreceptors.