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Flashcards in Regulation of ECF Volume 1 Deck (32):

What is one of the most important aspects of the ECF regulated by the kidney?

Its volume

ECF volume largely determined by body Na+


What determines the amount of H2O in any body component?

H2O can freely cross all cell membranes, the body fluids are in osmotic equilibrium, so that the distribution of TBW between cells and ECF is determined by the number of osmotically active particles in each compartment.

Na+ and Cl- are the major ECF osmoles.

K+ salts are the major ICF osmoles



How is body water distributed?

Of total body water (TBW)

1/3 in ECF
-Interstitial Fluid

2/3 Intracellular fluid (ICF)


What do changes in Na+ content effect?

Changes in ECF volume and therefore

-> Effect volume of blood perfusing the tissues = effective circulating volume and therefore BP


How are changes in Na+ detected by vasculature?

Think of what Na+ effects

Changes in Na+ content of ECF changes ECF volume

-> Plasma volume
-> Bloop Pressure

Regulation of Na+ is basically dependent on high and low P baroreceptors


Describe how increased salt and H2O loss as in vomiting, diarrhoea or excess sweating effects the sympathetic system?

Decreased ECF volume (hypovoleamia)

Decreased plasma volume,
Decreased venous pressure,
Decreased venous return,
Decreased atrial pressure,
Decreased EDV,
Decreased systolic volume,
Decreased cardiac output,
Decreased Blood pressure,

Carotid sinus baroreceptor inhibition of sympathetic discharge,

Incaresed sympathetic discharge
Incraesed venoud return
Increased vasoconstriction,
Increased TPR,
Increased blood pressure


When blood pressure decreases atrial pressure will decrease

What effects can this have?

Low P baroreceptors decrease discharge -> loss of tonic inhibitory discharge of ADH secreting neurones

Increase in ADH


When blood pressure decreases carotid sinus pressure will decrease

What effects can this have?

Decrease baroreceotor discharge -> decrease inhibition of sympathetic system

Sympathetic system effects on vasculature

Increased renal arterial constriction and incraesed Renin production
-> Increased angiotensin II


What effects does Incraesed angiotensin II have?

Increased proximal tubule NaCl and H2O reabsorption

Increased aldosterone
-> increased distal tubule NaCl and H2O reabsorption


How does angiotensin II effect how much Na+ is reabsorbed from the renal tubules?

Decreases peritubular capillary hydrostatic P (+ the increased osmotic pressure due to decreased water)

Increased Na+ reabsorption from the proximal tubule and therefore less Na+ excreted

Also causes release of aldosterone which increases distal tubule Na+ reabsorption


What is the overall effect of incraesed sympathetic discharge on the kidneys?

Increased renal vasoconstrictor nerve activity

Increased renal arteriolar constriction
-Reduced peritubular hydrostatic pressure
-Helps effect of increased osmotic tubule pressure

Increased renin
-Increased angiotensin due to renin
-Increased aldosterone due to angiotensin


How does increased tubular osmotic pressure occur and what effect does it have?

Loss of NaCl and H2O

Glomerular filtrate is more osmotic

Higher osmotic pressure in proximal tubule

Incraesed Na+ reabsorption because of greater reabsorptive forces in peritubular capillaries


How much can reabsorption in the proximal tubule change because of changes in starling's forces?

65% reabsorption in volume excess to 75% reabsorption in deficit

Big range in volume just due to changes in starling's forces


How is GFR effected by the effects of the sympathetic system, Renin and Angiotensin?

GFR remains largely unaffected

Autoregulation maintains GFR and the vasoconstriction of afferent and efferent means little effect on GFR until volume depletion severe enough to cause considerable decrease in mean blood pressure


How does autoregulation help in hypovoleamia?

In hypovolaemia there is an automatic readjustment of starlings forces in peritubular capillaries to increase amount of NaCl and H2O reabsorbed (increased oncotic pressure)

Also efferent arteriole constriction by angiotensin II


What are the autroregulation results of hypervolaemia?

Increased peritubular capillary pressure so efferent arteriole relaxation

Oncotic pressure reduced so less NaCl and H2O reabsorbed


What regulates distal tubule Na+ reabsorption?

Adrenal cortical steroid hormone, aldosterone

Very important in the long term regulation of Na+ and ECF volume


How is aldosterone secretion controlled?

Reflexes involving the kidneys themselves



What is the juxtaglomerular apparatus?

Smooth muscle of the media of the afferent arteriole, just before it enters the glomerulus has become specialised, containing large epithelial cells with plentiful granules = Juxtaglomerular cells (JG)

They are closely associated with a histologically specialised loop of the distal tubule = the macula densa.

The two together form the juxtaglomerular apparatus


What do juxtaglomerular cells produce?


A proteolytic enzyme which acts on a large protein in the a2-globulin fraction of the plasma proteins = angiotensinogen


What does renin do?

Renin splits off the decapaptide angiotensin I which is then converted by enzymes in the endothelium to the active octapaptide = angiotensin II

Angiotensinogen in the plasma ---Renin---> angiotensin I


What does angiotensin converting enzyme (ACE) do?

Angiotensin I ----ACE---> angiotensin II


Where is ACE found?

Throughout the vascular endothelium, but the greatest proportion of the conversion occurs as the blood passes through the pulmonary circuit, but all of the endothelium is important.


How does angiotensin II stimulate aldosterone secretion?

Angiotensin II stimulates the aldosterone- secreting cells in the zona glomerulosa of the adrenal cortex


What is the rate limiting step in RAAS?

The rate limiting-step is the release of renin since angiotensinogen is always present in plasma


What controls renin release?

1. Increased renin release when P in afferent arteriole at the level of the JG cells decreases

2. Increased sympathetic nerve activity via B1-effect

3. Rate of renin secretion is inversely proportional to rate of delivery of NaCl at the macula densa (specialised distal tubule)

4. Angiotensin II feeds back to inhibit renin

5. ADH inhibits renin release (osmolarity control)


How do JG cells detect pressure in afferent arteriole?

Act as renal baroreceptors

Less distension -> increased secretion of renin.

Intrinsic property, occurs if denervated


How does decreased NaCl delivary at the macula densa effect renin release?

Increased renin release

Macula densa cells are sensitive to [NaCl] in the late thick ascending limb.

Decrease in [NaCl] initiates a signal from the macula densa that has two effects:
1. Decreases resistance to blood flow in the afferent arterioles via vasodilation, which increases GFR toward normal
2. Increases renin release from the juxtaglomerular cells of the afferent and efferent arterioles, which are the major storage sites for renin.


What structural feature allows tubuloglomerular balance to be easily controlled?

Close relationship between afferent arteriole with JG cells and macula densa provides mechanism for controlling input and output of tubules and basis of tubuloglomerular balance


In hypovolaemia, increased proximal AND distal tubule Na+ reabsorption together with osmotic equivalents of H2O, helps restore volume deficits, mediated by CV reflexes.

Why is angiotensin II fundamentally important in the body's response to hypovolaemia?

1. Stimulates aldosterone and therefore NaCl and H2O retention.

2. It is a very potent biological vasoconstrictor, 4-8x more potent than NE, therefore contributes to increased Total Peripheral Resistance.

3. It acts on the hypothalamus to stimulate ADH secretion -> increasing H2O reabsorption from the collecting duct

4. It stimulates the thirst mechanism and the salt appetite (in the hypothalamus)


Consider a person suffering from severe diarrhoea, who has lost 3L of salt and water (from ECF) and drinks 2L of pure water.

Decrease in ECF osmolarity as more net salt lost than net water -> Inhibition of ADH via osmoreceptors

Decrease in ECF volume -> increased ADH via baroreceptors

How is this overcome?

Volume considerations have primacy if ECV is compromised, so that ADH will increase because of the baroreceptors, even though this is associated with hypo-osmolarity

ECF osmolarity will effect [ADH] when small changes occur.

When ECF volume is threatened though other mechanisma will occur
-> "emergency mechanism for the brain


What is normally the main determinant of [ADH]?


But if sufficient volume change to compromise brain perfusion, then volume becomes the primary drive, so to conserve volume, tolerate disturbed osmolarity.

Once volume is restored in hypovolaemia, then osmolarity will be normalised and again becomes main determinant of ADH.