Sodium and Potassium - part of Tubular Function - have been through. Flashcards
What happens to ECF volume if you have prolonged high sodium diet?
Retain more water, and therefore gain weight (you gain water to keep osmolarity constant). This leads to increased blood pressure, and blood volume. The opposite happens for decreased dietary sodium.
State the relative amounts of sodium reabsorbed in different parts of the nephron.
65% - PCT 25% - loop of Henle 8% - DCT Up to 2% - collecting duct
Describe the relationship between GFR and sodium reabsorption.
The greater the GFR the greater the sodium reabsorption, but proportions remain the same.
How is Na+ reabsorption increased in the nephron and Na+ levels preserved? (x5 components of the mechanism)
- LOW BLOOD PRESSURE increases sodium reabsorption by REDUCING GFR; so more Na+ retained in blood rather than entering filtrate which increases water retention.
- Low GFR also promoted by SNS activity - which causes vasoconstriction of afferent arteriole, so less blood reaches the nephron.
- Another effect of increased SNS means PCT reabsorbs more sodium.
- SNS activity activates juxtaglomerular apparatus –> grannular cells secrete renin which increases Angiotensin II. Angiotensin II (increases blood pressure by vasoconstriction and) stimulates uptake of Na+ in PCT.
- Angiotensin II also increases aldosterone levels which affects DCT and collecting duct by increasing Na+ uptake.
- Low tubular sodium at juxtaglomerular apparatus also increases production of renin which increases angiotensin II and aldosterone – to mediate the same effects described above.
——-> Overall effect = raised BP (because sodium reabsorption results in passive flow of water to balance osmolarity.
What triggers the juxtaglomerular apparatus to produce renin? (x3)
Low tubular Na+ concentration Low renal perfusion pressure. SNS activity.
What hormone is involved in decreasing sodium reabsorption? What is the mechanism? (x4 components)
Atrial naturietic peptide increases GFR by by (i) increases diameter of afferent (and systemic blood vessels), and constricts efferent arteriole; (ii) reduces PCT activity; (iii) suppresses renin release at juxta apparatus; (iv) reduces Na+ reabsorption in collecting tubules esp. thick ascending limb.
OVERALL AIM IS TO REDUCE BLOOD PRESSURE.
Describe process of renin release? Triggers? (x3)
Activity of Na+/K+/Cl- channel in DCT senses amount of salt in the system at macula densa.
–> If there’s not much salt, amount of sodium going into tubule cells falls. Therefore, cells have a low osmolarity compared to the envoiroment they’re sat in, so water moves out into interstitium. They therefore shrink, and thus produce PGe2 and NO, stimulates release of renin from glomerular cells.
—> (As well as low osmolarity) ALSO STIMUALTED BY SNS AND HORMONES.
Where do you find a lot of ACE? REMINDER - what is the function of ACE?
Lung Endothelium. REMINDER: ACE converts Angiotensin I to Angiotensin II.
What effect does angiotensin II have? (x3) In each case, where does it effect?
(1) Increase sodium reabsorption in the PCT. Subsequently increases water reabsorption = increased BP.
(2) Vasoconstriction –> also increases BP.
(3) Increases aldosterone synthesis in adrenal glands.
To stimulate Na absorption, what 3 stimuli?
decrease blood pressure, decrease fluid volume, increase sympathetic stimulation
Describe the effects of aldosterone on absorption and secretion. (x3)
Increase Na+ reabsorption, Increases H+ secretion, Increases K+ secretion
What is the result of aldosterone excess?
Hypokalemic Alkalosis
Which cells does aldosterone work on
Principal cells in the collecting duct (and DCT).
How does aldosterone work? How does it cause an increase in sodium reabsorption? (x3 effects)
Aldosterone is a steroid so it has a genomic effect.
–> binds to steroid hormone receptor in cytoplasm (type 1 intracellular receptors).
—> It relocalises the vesicles containing sodium transporters to the apical membrane.
–> It also increases transcription and production of more sodium channels and Na+/K+ ATPase on basolateral membrane and Na+ channels on apical membrane.
–> increase expression of regulatory proteins which open the Na+ channels on the apical membrane.
RESULT: increase sodium reabsorption.
What are the consequences of hypoaldosteronism?
(1) Reabsorption of sodium in the distal nephron is reduced (2) Increased urinary loss of sodium (3) ECF volume falls (4) Increased renin and Angiotensin II and Vasopressin secretion.
what are the symptoms of hypoaldosteronism?
Low blood pressure, dizziness, palpitations, salt craving.
What are the consequences of hyperaldosteronism?
(1) Increased sodium reabsorption in the distal nephron. (2) Reduced urinary loss of sodium (3) ECF volume increases - HYPERTENSION (4) Reduced angiotensin and vasopressin secretion (5) Increased ANP and BNP (niuretic peptide).
What is Liddle’s Syndrome?
Mutation in the aldosterone dependent Na+ channel - the channel is permanently switched on resulting in sodium retention from constant sodium reabsorption; which leads to HYPERTENSION
what are the symptoms of hyperalldosteronism?
High blood pressire, muscle weakness, polyuria and thirst.
What does low pressure stimulate?
RAS - more angiotensin II produced Increase sympathetic activity Increase ADH release
How is ANP produced and what does it do?
ANP is produced by atrial stretch It causes vasodilation of renal blood vessels Inhibition of sodium absorption in the PCT and in collecting ducts Inhibits release of renin and aldosterone