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At what vertebral level is the hilum of the kidney?
- - L1.
- - L1 corresponds to inferior aspect of hilum on left kidney, superior aspect of hilum on right kidney
Describe the arterial blood supply of the kidney
- - Renal artery > segmental arteries > interlobular arteries > arcuate arteries > radial arteries
- Renal artery > uteric branch
Nervous innervation of kidneys?
- - Celiac plexus > travels along renal artery to form renal plexus
- - Also receives input from lower thoracic and lumbar splanchnic nerves
Name the 3 cell types of the juxtaglomerular complex?
- - Juxtaglomerular cells
- - Macula densa
- - Extraglomerular cells
Briefly describe the Renin-Angiotensin-Aldosterone Sytem
1. Juxtaglomerular cells secrete renin
2. Renin converts angiotensinogen to angiotensin in liver
3. Angiotensin is cleaved into angiotensin II by ACE in the lung capillaries
4. AII acts on zona glomerusa cells to instigate secretion of aldosterone in adrenal cortex.
Which areas of the nephron do angiotensin II, aldosterone and ADH act?
What are their basic mechanisms of action?
- - AII acts on PCT. Increases Na+ & H20 reasbsorption
- - Aldosterone acts on DCT. Increases Na+ & H20 reasbsorption
- - ADH acts on CD. Increases H20 reabsorption only
Mechanism of action of aldosterone?
- - Acts on principal cells of cortical CD in nephron
- - Stimulates Na/K ATPase on basolateral membrane; increasing Na+ reabsorption and K+ excretion
ADH: stimulus for secretion and mechanism of action?
- - Secreted in response to increased plasma osmolarity OR fall in MAP detected by carotid/aortic baroreceptors
- - Acts on V1 receptors in blood vessels causing smooth muscle vasoconstriction
- - Acts on V2 receptors in CD, causing cAMP activation and upregulation of AQ2 into luminal membrane. Water is freely permeable in basolateral membrane.
Factors causing renin release:
- - Low BP at kidney
- - Low tubular Na+ levels
- - Hypokalaemia
NSAIDs inhibit prostaglandins. What effect will this have on blood pressure?
- Prostaglandins regulate the tone of the renal arterioles.
- Inhibition of prostaglandins can cause renin release and thus resultant Na+ and H20 reabsorption, increasing BP.
Where else in the body (aside from kidney) are aldosterone receptors found?
- Colon; illustrating its importance in regulating fluid levels.
Hormones involved in reducing blood pressure (antagonists of RAAS/ADH) and Na+ levels:
- - ANP
- - BNP
- - Kinins
- - Renal prostaglandins
- - Dopamine
Factors influencing release of ADH:
- - Stress
- - Cortisol
- - Decreased blood volume/pressure
- - Increased plasma osmolarity
- NB - Alcohol inhibits release of ADH
Equation for Mean Arterial Pressure?
- MAP = Q x TPR
- MAP = Mean Arterial Pressure
- Q = Cardiac Output
- TPR = Total Peripheral Resistance
What is the physiological response of the afferent arteriole to an increase in MAP?
- 1. Stretch of vascular smooth muscle cells of afferent arterioles activates stretch-senstive Ca2+ permeable channels.
- 2. Cytosolic Ca2+ increase triggers smooth muscle contraction.
- 3. Afferent arteriole vasoconstricts, reducing renin secretion
Briefly describe tubuloglomerular feedback during elevated MAP.
- 1. Increased MAP causes increased GFR. Thus an increase fluid flow to DCT.
- 2. Increased Na+ uptake into macula densa cells of DCT stimulates adenosine release from macula densa.
- 3. Adenosine triggers vasoconstriction of afferent arteriole - reducing the GFR.
- 4. Adenosine also inhibits renin secretion from granular cells.
A decrease in blood volume activates the sympathetic nervous system. What are the responses of this sympathetic activation?
- - Increases PCT Na+/H+ exchange
- - Vasoconstriction of arterioles (efferent > afferent)
- - Inreased renin secretion
Effects of ANP?
- - Decreases DCT Na+ transport
- - Vasodilation of arterioles (afferent > efferent)
- - Inhibits renin and aldosterone secretion
Briefly describe the physiological cause of diabetic nephropathy.
- 1. Increased glucose concentration in glomerular capillaries leads to an increased glucose concentration in the PCT.
- 2. This causes increased activity in the Na+/glucose transporter (luminal membrane); leading to increased glucose and Na+ reabsorption across basolateral membrane.
- 3. This Na+ pulls water across the membrane with it.
- 4. Downstream in the tubule, this causes a pressure decrease in the PCT.
- 5. The decrease in flow to the macula densa activates tubuloglomerular feedback
- 6. Leads to hyperperfusion; increased GC blood pressure
Poorly controlled diabetes leads to increased glomerular pressure. How does this instigate the pathological process of diabetic nephropathy?
- - Increased glomerular pressure leads to increased matrix deposition and hypertrophy/proliferation of mesangial cells.
- - Formation of glomerular nodules/scarring
- - Eventually leads to compression of glomerular cpaillaries and decreases in GFR.
- NB - tuboglomerular feedback can further exacerbate kidney damage.
How would you treat inappropriate tuboglomerular feedback caused by diabetic nephropathy?
- Treat with ACE inhibitors such as ramipril to reduce deleterious effects of the positive feedback loop.