ECF volume regulation Flashcards
What is the main regulatory of ECF volume
Regulation of Na+
What is causes of hyovoleaemia (decreased ECF volume)
Increased salt and H2O loss can be caused by:
Vomiting
diarrhoea
excess sweating
What is the cardiovascular reflex to a decrease in plasma volume in hypovolaemia
Decreases in: Venous pressure—> Venous return—> Artrial pressure –> End diastolic volume—> stroke volume —> blood pressure
This decreases in blood pressure, decreases the high pressure baroreceptors inhibition of sympathetic discharge, therefor sympathetic discharge in increased
Increasing sympathetic vasoconstrictor, increasing total peripheral resistance, and increasing blood pressure back towards normal
How does the cardiovascular reflex to hypovalemia affect ADH secretion
Causes a decrease in atrial pressure and carotid sinus baroreceptors discharge, therefore stimulating increase in secretion of ADH
How is GFR maintained in hypovalemia
Due to autoregulation
The cardiovascular reflex causes sympathetic discharge which causes the renal arteriolar to constrict,
this is then coupled with angiotensin II which mediates the constriction of efferent,
so Vasoconstrictor of afferent and efferent means little effect on GFR until volume depletion sever enough to cause considerable decrease in mean arterial pressure
What is the specific function of the kidney in hypovalemia
Increase reabsorption of Na+ by peritubular capillaries
Produce renin which stimulates angiotensin II production
How does the rate of Na+ uptake in peritubular capillaries change in hypovalemis
Due to Readjustments of starling forces in pertibubular capillary: decreased pertiubular capillary hydrostatic pressure and the increased osmotic pressure more than normal due to loss of NaCl and H2O
causing greater reabsorption due to greater reabsorption forces in peritubular capillaries determined by the osmotic pressure
Where and how much Na+ is reabsorbed in hypovalemia
Can reabsorb up to 75% of the filtrate at the proximal tubule
What stimulates the release of renin in the kidney
Decreased blood pressure means pressure in afferent arteriole at the level of the juxtaglimeualr cell decreases causing decreased distension, resulting in secretion of renin
Increased sympathetic nerve activity, as beta i receptors cause vasoconstriction, increases renin production
Decreased NaCL delivery in specialised distal tube the macula densa
What is the action of the renin hormone
A proteolytic enzyme which acts on angiotensin, to split it of into from angiotensin I
What is angiotensin and where is it produces
A decapeptide present in the plasma and constantly produced from the liver
What converts angiotensin I and angiotensin II
ACE enzymes found in the vascular epithelium
Where is renin hormone secreted in the kidney
Juxtaglomerular cells
What inhibits renin secretion
ANP (atrial natriuretic peptide) - lower BP
The macula densa detecting high rate of delivering NaCl,
angiotensin feedsback to inhibit renin
ADH inhibits renin release - for osmolarity control
What is the juxtaglomerular apparatus
Juxtaglomerular cells plus the macula densa
What is the macula densa
The macula densa is a collection of specialized epithelial cells in the distal convoluted tubule that detect sodium concentration of the fluid in the tubule,
so its main function is to regulate blood pressure and the filtration rate of the glomerulus
What is the juxtaglomerular cells
Smooth muscle media of the afferent arteriole, just before it enters the glomerulus has become specialised and contains large epithelial cells with plentiful granules that release the hormone renin
What is the benefit of the juxtaglomerular cells plus the macula densa
The close relationship between the juxtaglomeualr cells and macula densa, creates a tubuloglomerular feedback which affects the GFR and controls the rein rate of production
What is the rate of renin production inversely proportional to
The rate of secretion is inversely proportional to the rate of delivery of NaCL at the macula densa
eg decreased delivery of NaCl increases renin production
How does tubuloglomerular feedback contribute to GFR constancy
As in increased GFR, causes the flow in tubules to increase and therefore increase in the macula densa, this causes paracrine hormone from macula densa go to afferent arteriole, causing it constrict, so the resistance in the afferent arteriole increase, so hydrostatic pressure in glomerulus decreases meaning the GF decreases
The main function of renin is the production of angiotensin II, where does angiotensin have an effect
arterioles
cardiovascular control centre in medulla
hypothalamus
adrenal cortex
what is the affect of angiotensin II on the arteriole
Cause vasoconstriction, therefore increase blood pressure
what is the affect of angiotensin II on the cardiovascular control centre in the medulla
Increase cardiovascular reflex to increase blood pressure
what is the affect of angiotensin II on the hypothalamus
Increase ADH - so increase volume and maintain osmolarity to increase the blood pressure
Stimulate thirst mechanism and salt appetite
what is the affect of angiotensin II on the adrenal cortes
The angiotensin II produced stimulates the aldosterone secreting cells in the zona glomerulosa of the adrenal cortex to increase aldosterone
What is the affect of aldosterone
Aldosterone passes in the blood to the kindey where it then stimulates the distal tubular Na+ ion reabsorption
20% reabsorbed, increasing volume and maintains osmoloraity
How does the kidney help to restore volume deficits mediated by the CV reflex in hyovalemia
Due to the overall the increasesed proximal and distal tubule Na+ reabsorption together with osmotic equivalents of H2O
What affect on ADH secreting cells would occurs when you ECF volume decreases but you also have hyposomolarity
eg diarrhoea 3L loss then drinking 2L of pure water
Opposing inputs
ECF volume decreases would cause increase of AH secretion via baroreceptor
Hyposmolarity would cause inhibition of ADH secretion via osmoreceptors
In the situation of decreased ECF volume with hyposomolarity what takes priority and why
Normally osmolarity is main determinant of ADH concentration but if there is sufficient volume changes to compromise brain perfusion then volume becomes primary drive
acts as an emergency mechanism to save perfusion for the brain
What then occurs indecreased ECF volume with hyposomolarity when volume becomes primary drive
therefore ADH will increase because of the baroreceptors as aim to conserve water and tolerate disturbed osmolarity and once volume is restored, the osmolarity will then be normalised
Where does sodium absorption occur and what is the percentage of absorption there
65-75% of NaCl and H2O reabsorbed from proximal tubule
15-20% of NaCl and H2O reabsorbed from the loop of henle
5-20% of NaCl reabsorbed from distal tubule and collecting duct
What hormone promotes sodium reabsorption and where
Aldosterone promotes Na+ reabsorption in the distal tubule
What is aldosterone hormone also responsible for inn the distal tubule
Potassium secretion
Why is weight gain seen due to excess aldosterone
as increased Na+ reabsorption causes weight gain due to increased H2O and Na+ retention, increasing the volume
Why would spontaneous diereses occur in excess aldosterone
As ANP overrides aldosterone effects
because the volume expansion due to NA+ reabsorption weight gain stimulates the release of ANP from atrial cells, causing spontaneous diuresis secondary to aldosterone volume expansion
Why are patients with hyperaldoteronsim (excess aldosterone) depleted of K+ but don.t have a high sodium level
As when spontaneous diuresis occurs when ANP overrides aldosterone, it cause loss of Na+ and h2O, but aldosterone still continue K+ loss, because still increase K+ secretion
What syndromes is associated with excess aldosterone
Conns syndrome
What hormone promotes Na+ excretion
ANP (atira naitriuretic peptide)
What causes secretion of ANP and where is it secreted
Increased blood/ECFvolume causes increased atrial stretch of myocardial cells, realising ANP
What is the overall affect of ANP
Natriuresis - loss of H2O and Na+ in urine
Decreases blood pressure
Where does the hormone ANP affect
hypothalamus
kidney
Adrenal cortex
medulla oblongata
What is the affect on ANP on the hypothalamus
Inhibits ADH, so increases NaCl and H20 Excretion
What is the affect on ANP on the kidneys
Increase GFR,
Decreases Renin (as opposes the actions of angiotensin II)
- Less aldosterone so increases NaCl and H20 Excretion
- decreased blood pressure
What is the affect of ANP on the adrenal cortex
- Less aldosterone so increases NaCl and H20 Excretion
What is the affect of ANP on the medulla oblongata
decrease blood pressure
How does diabetes mellitus abolish interstitial gradient
As the high plasma level of glucose Tm
Glucose remains in tubule and extras osmotic affect to retain H2O, decreases osmolarity in tubule
The decreases passive diffusion of sodium due to reduced concentration gradient, therefore further prevents NaCl pumps in the loop of henle
This means the movement of H2O out of tubules into the interstium is reduced as no concentration gradient is created as sodium remains in tubule
this means the medullary insterstial gradient is much less as there is a considerable reduction of NaCl and H20 reabsorbed from the loop of henle
How is glucose reabsorption further prevented in diabetes mellitus
As when reduces passive diffusion of sodium, further prevents glucose reabsorption as is a symport with sodium
Why is there a large volume of NaCl and H2O delivered to the distal tubule
As because of the high concentration of glucose in the tubules, it means that water and sodium is retained in the tubule with glucose and is not reabsorbed
What affect does the high volume of NaCl and H2O in the distal tube in diabetes mellitus cause
The body thinks a large volume of NaCl and H2O delivered to the distal tubule would mean there is excess ECF volume, rather than just a high volume of h20 and Na+ in ECF
So macula densa decreases renin secretion, further decreasing Na+ reabsorption at distal tube
further getting ride of NaCl and H2O
What further affect does wrecking the interstial gradient have in diabetes melitus
Decreases the ability of ADH to conserve water,
as water cant move out into the interstium from collecting ducts as It is driven by the hypertonic medullary interstitial gradient, created by the countercurrent multiplier of the loop of Henle which no longer exists
The mechanism of diabetes mellitus increasing the volume of NaCl and H2O delivered to the distal tubule, wrecking the interstice gradient has what affect on your urine output
Excrete 6-8L of isotonic urine/day ( large volume of urine produced)
= polyuria
How does diabetes mellitus cause a hyperglycaemia coma
The large volume or nealt isotonic urine will be excreted,This can cause severe salt and water depletion in Diabetic patients, which results in hypotension, which can can become severe when it result in inadequate blood flow to the brain which can cause a hyperglycaemia coma
What occurs in a hypoglycaemia coma
due to inadequate glucose for the brain
How is thirst one of the first sign of diabetes mellitus
This can cause severe salt and water depletion in Diabetic patients and if ingestion is not enough will trigger thirst mechanism
= polydipsia
