Lecture 30: Renal 4- The Role Of Kidneys In Na+ And K+ Balance Flashcards
Why do you have to regulate sodium?
If sodium is retained, water will be retained and extra cellular fluid volume will increase.
- plasma is part of ECF
- regulating sodium excretion in the Rhine is the main means of regulating ECF and blood volume
- regulating blood column is the most important means if long-term regulation of blood pressure.
- renal regulation of sodium balance occurs by changin renal reabsorption (not secretion)
What are the ins and out for sodium ie sodium balance
Input: sodium in diet
Out: skin (sweat, burns, haemorrhage)
-gastrointestinal losses (diarrhoea, vomiting, drainage)
-kidneys (most of loss)
Tell me how sodium is reabsorbed
Normally 99% of filtered Na+ is reabsorbed.
1. 65% unregulated in Proximal tubule
2. 25% in ascending limb of LOH
3. Small amount (4->9%) in DT and Collecting duct under hormonal control: aldosterone and atrial natriuretic peptide
Slide 7
Renin- angiotensin- aldosterone system (RAAS)
Most important mechanism for regulating Na+ reabsorption in the kidneys and long-term regulation of BP.
This system involves 2 enzymes- renin and ACE and 2 hormones- angiotensin 2 and aldosterone
Tell me about aldosterone.
What are its cellular effects?
- steroid hormone produced/released at adrenal cortex (outer part of adrenal gland)
- aldosterone release is end result of the renin-angiotensin-aldosterone-system.
- release stimulated by presence of angiotensin 2 (and by increased plasma K+)
- increased Na+ reabsorption and K+ secretion In distal nephron (DT and CD)
- indirectly leads to increased water reabsorption through increased ECF osmolarity
Cellular effects:
-aldosterone acts on the distal tubule and CT
-it causes the synthesis of new Na+ channel and new K+ channels which are inserted into luminal membrane
-and new Na/K pumps which are inserted into the basolateral membrane
-so it increases Na* reabsorption and K+ secretion
Angiotensin increases mean arterial pressure!
Check out slide 11
Renin-angiotensin-aldosterone system (RAAS)
-renin released from the kidneys initiates this process. It is the rate-limiting step
-the amount of renin secreted determines how much angiotensin 2 and aldosterone will be present in the blood
Slide 12
Juxtaglomerular apparatus
- renin is secreted from the juxtaglomerular apparatus of the kidney
- located where the start of the distal tubule passes between the afferent and efferent arteriolar
- 2 specialised cell types:
- macula densa cells in wall of the DT
- juxtaglomerular cells on wall of afferent arteriole-specialised vascular smooth muscle cells
Juxtaglomerular cells secret refine which initiates the RAAS
How is renin release regulated?
- reduced MAP is the primary stimulus for renin release via:
1. Decreased stretch at afferent arteriole
2. Baroreceptor reflex stimulating sympathetic nerves
3. ⬇ GFR, reducing delivery of fluid to macula densa cells
Increased MAP will reduce renin release
Slide 14
Juxtaglomerular apparatus
Macula dens cells monitor flow rate through DT
In response to ⬇ flow rate macula densa cells: do what?
- Secrete vasodilator to dilate afferent arteriole= tubuloglomerular feedback for autoregulation of GFR
- Signal to JG cells to increase renin secretion (activation of RAAS and systemic regulation of MAP)
Atrial natriuretic peptide (ANP) does what? And how does it do it?
Inhibits sodium reabsorption
-secreted from the atrial walls of heart in response to stretch associated with plasma volume.
ANP decreases renal absorption of Na+ by:
- limiting the number of open Na+ channels in luminal membrane of principle cells
- inhibition of RAAS: decreases ⬇ rein secretion from kidney and aldosterone from adrenal cortex
ANP increases filtration (and excretion) of sodium:
- increases in GFR (dilates afferent/ constricts efferent arterioles).
- note that autoregulation of GFD will limit this effect
Learn the shit out of the table on slide 19
Do it
Why do you have to regulate plasma K+ levels?
- insignificant effect on blood volume or osmolarity.
- affects resting membrane potential of cells
- Normal plasma K+ concentration= 3.5-5mM
- ⬆plasma K+ (=hyperkalaemia) depolarises cells. Increased APs initially but can’t depolarises fully so become less excitable➡ cardiac arrhythmias and muscle weakness (>6mM) and death (>7mM)
- ⬇plasma K+ (=hypokalaemia) hyperpolarizes the cells ➡ muscle weakness (<1mM)
Tell me about the normal potassium balance. How its maintained?
- balance of intake and output maintained by kidneys
- approximately 98% lf potassium in body is intracellular
- short term regulation by cellular uptake
- long- term regulation by kidneys
Regulation of plasma K+ by cellular uptake
- in the short term we regulate plasma K+ by dumping excess K+ Into the cells
- insulin stimulates uptake of K+ into cells after a meal
- adrenalin stimulates uptake of K+ into cells
- important during exercise and tissue damage
Renal handling of K+
K+ is freely filtered at glomerulus with both reabsorption and secretion occurring along the tubule
- Unregulated reabsorption from PT (55%) and ascending LOH (30%)
- Regulated secretion in late distal tubule and collecting duct is diet dependant
Long term regulation of Plasma K+ occurs through secretion in distal nephron (DT & CD)
