Lecture 7 Salt and water balance Flashcards
What are the hormones that regulate tubular reabsorbtion?
Aldosterone
Angiotensin II
Antidiuretic hormone
Atrial natriuretic peptide
Parathyroid hormone (not yet needs to be known)
What does Aldosterone do?
Increases NaCl and H2O reabsorption and K+ secretion
What does Angiotensin II do?
NaCl and H2O reabsorption and H+ secretion
What does ADH do?
Reabsorbs water at distal tubule and collecting tubule+duct
What does Atrial Natriuretic Peptide do?
Decreases NaCl reabsorbtion at distal tubule and collecting tubule+duct
Where does parathyroid hormone act?
Acts on proximal tubule, thick ascending loop of henle, and distal tubule
What does parathyroid hormone do?
PO2 reabsorption and increased calcium absorption
How does water loss get controlled?
An increase in plasma osmolarity causes the ECF osmolarity to increase. This results in osmoreceptor cells shrinking which results in action potential which are relayed to posterior pituitary gland and this results in ADH release.
ADH results in water reabsorption and in turn an increase in plasma water which dilutes the plasma and the ECF
Where is ADH released?
In the posterior pituitary gland
Which brain regions are responsible for ADH release?
Supraoptic (5/6)
Paraventricular (next to 3rd ventricle of brain) (1/6)
What is ADH produced in response to?
Plasma osmolarity increase
Medullary BP centers (drop in BP)
Drop in blood volume
What factors decrease ADH release?
Low blood osmolarity
High blood volume
High blood pressure
How does aquaporin expression work?
The interstitial side aquaporins are always expressed and open and unregulated these maintain the cell’s osmolarity.
On the tubular side there are aquaporin 2 channels which get exocytosed into vesicles.
Vasopressin binds to the membrane receptor which activates cAMP secpnd messenger system.
Cell inserts AQP2 water pores into apical membrane.
Water is then absorbed into blood via osmosis
How is salt reabsorption controlled?
atII and aldosterone, these hormones have little effect on Na+ concentration except under extreme conditions.
This is called RAAS (Renin-angiotensin-aldosterone-system)
When is renin typically produced?
In the kidney by the juxtaglomerular apparatus
Why is renin produced?
In response to low GFR (i.e low BP)
How does the renin angiotensin pathway work?
Kindeys produce renin
Liver produces angiotensinogen
renin converts angiotensinogen into angiotensin I
Surface of pulmonary and renal endothelium contains Angiotensin Converting Enzyme which converts AtI into AtII which has systemic effects to raise BP
How does the renin angiotensin pathway work?
Kindeys produce renin (rate limiting part of process)
Liver produces angiotensinogen constantly
renin converts angiotensinogen into angiotensin I
Surface of pulmonary and renal endothelium contains Angiotensin Converting Enzyme which converts AtI into AtII which has systemic effects to raise BP
How does AtII raise BP?
Increases sympathetic activity
Increases tubular reabsorption of Na Cl and H2O. It also increases excretion of K+ (through sodium potassium pump activity increase)
Adrenal gland and cortex produce more aldosterone which increases H2O reabsorption as well as salts
Areteriolar vasoconstriction increases TPR which increases MAP and in turn blood pressure
ADH secretion resulting in more H2O reabsorption at collecting duct
Where is aldosterone produced?
Adrenal cortex
What is the negative feedback of the Renin Angiotensin Aldosterone System?
Renin release is slowed down in response to the increase in BP
How does renin get secreted?
Granular cell of the juxtaglomerular apparatus produces it in response to salt receptors in the macula densa cells which sense change in electric potential and respond.
a decrease in salt concentration
What are the triggers for increased renin release?
Drop in NaCl concentration at DCT.
Decrease in stretch on the afferent arterioles
Increase in sympathetic stimulation (as a result of the baroreceptor reflex)
What is the most potent sodium retaining hormone?
AtII
What does AtII do that makes it so powerful at retaining sodium?
Directly stimulates basolateral Na+/K+-ATPase and Na+/H+ exchange in PCT.
Increases reabsorption by peritubular capillaries.
Stimulates aldosterone secretion
Where is aldosterone produced?
Adrenal cortex zona glomerulosa
What mediates adrenal secretion of aldosterone?
Mostly AtII
And local potassium concentration
also ACTH
Why is aldosterone produced when its effects are similar to AtII?
It is a steroid and its effect is more long term.
What does aldosterone do in cells to increase BP?
Increases sodium reabsorption and secretion of potassium and hydrogen
Increases active reabsorption of sodium (water follows)
Increases BP and blood volume
Where are principle cells located?
Towards end of nephron so in collecting tubule
What does aldosterone bind?
Mineralocorticoid receptor which activates signal transduction and gene transcription and non-genomic activation.
Acts on principle cells of cortical convoluted tubule by stimulating the basolateral sodium potassium pump
It also increases the sodium permeability of luminal membrane
and sodium potassium + sodium hydrogen counter transporters.
Why is potassium secreted?
To maintain electrochemical gradient and H+ cant be released to maintain pH
What does Atrial Natriuretic peptide do?
Decreases Na+ and H2O reabsorption and inceases urinary loss and drops blood volume
increases GFR by dilating afferent arteriole and constricting efferent arteriole
What does ANP get released in response to?
High atrial pressure indicates high venous pressure and in turn high venous volume
What is the response of cells to ANP?
Decreases ADH release
Decreases renin release and in turn aldosterone
Decreases GFR
Decreases aldosterone directly as well
Stimulates medulla to decrease BP
AS A RESULT INCREASES NACL AND H2O EXCRETION
Where is potassium stored?
98% is stored in the ICF (prevents it from becoming problematic)
Why is potassium regulated so precisely?
High blood potassium results in heart problems and nervous system problems.
How is potassium regulated?
Excreted from kidneys
ECF:ICF distribution (store some in the cells)
What factors shift K+ into cells?
Insulin
Aldosterone
Beta-adrenergic stimulation
Alkalosis
What factors shift K+ out of cells?
Insulin deficiency
Aldosterone deficiency
Beta-adrenergic blockade
Acidosis
Cell lysis
Strenuous exercise
Increased extracellular fluid osmolarity
How is potassium secreted?
Principle cells
How is potassium secretion determined?
Sodium potassium ATPase activity. More sodium reabsorption means more potassium excretion.
Potassium electrochemical gradient
Potassium permeability.
There is also a H+/K+ ATPase co transporter which has minimal effect but alkalosis can result in loss of potassium
How is potassium controlled by feedback?
Increase in extracellular potassium concentration increases potassium secretion in 3 ways
Na+/K+-ATPase stimulation
Increase in K+ gradient towards tubule
Increase in aldosterone secretion
What is drinking threshold determined by?
Osmolarity changes .
How is blood volume regulated?
Low P baroreceptors in great veins and right atrium detect low volume
Hypotension is detected by high P baroreceptors.
AtII is a very potent dipsogen
All these symptoms feed into hypothalamus
How does AtII cause thirst?
AtII is a neurotransmitter in the hypothalamus used to influence thirst
What controls thirst?
Thirst increased by: Increase in osmolarity Drop in Blood volume Drop in BP Rise in AtII Dryness of the mouth
Thirst decreased by: Decrease in osmolarity Increase in blood volume Increase in blood pressure Drop in AtII Gastric distention
What region of the brain controls water balance?
Thirst center in the anteroventral 3rd ventricle region. Lesion causes acute adypsia (absence of thirst)
Where are the osmoreceptors located?
AV3V (anteroventral 3rd ventricle region.)
What is the stimulus in hunger for salt?
Drop in sodium concentration in extracellular fluid
BP drop increases salt appetite
