Kidney

• - L1.
• - L1 corresponds to inferior aspect of hilum on left kidney, superior aspect of hilum on right kidney

• 
• - Renal artery > segmental arteries > interlobular arteries > arcuate arteries > radial arteries

- Renal artery > uteric branch

• - Celiac plexus > travels along renal artery to form renal plexus
• - Also receives input from lower thoracic and lumbar splanchnic nerves

• - Juxtaglomerular cells
• - Macula densa
• - Extraglomerular cells

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.

• - AII acts on PCT. Increases Na⁺ & H₂0 reasbsorption
• - Aldosterone acts on DCT. Increases Na⁺ & H₂0 reasbsorption
• - ADH acts on CD. Increases H₂0 reabsorption only

• - Acts on principal cells of cortical CD in nephron
• - Stimulates Na/K ATPase on basolateral membrane; increasing Na⁺ reabsorption and K⁺ excretion

• - 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.

• - Low BP at kidney
• - Low tubular Na⁺ levels
• - Hypokalaemia

- Prostaglandins regulate the tone of the renal arterioles.

- Inhibition of prostaglandins can cause renin release and thus resultant Na⁺ and H₂0 reabsorption, increasing BP.

- Colon; illustrating its importance in regulating fluid levels.

• - ANP
• - BNP
• - Kinins
• - Renal prostaglandins
• - Dopamine

• - Stress
• - Cortisol
• - Decreased blood volume/pressure
• - Increased plasma osmolarity
• NB - Alcohol inhibits release of ADH

• MAP = Q x TPR
• Where:
• MAP = Mean Arterial Pressure
• Q = Cardiac Output
• TPR = Total Peripheral Resistance

• 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

• 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.

• - Increases PCT Na⁺/H⁺ exchange
• - Vasoconstriction of arterioles (efferent > afferent)
• - Inreased renin secretion

• - Decreases DCT Na⁺ transport
• - Vasodilation of arterioles (afferent > efferent)
• - Inhibits renin and aldosterone secretion

• 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

• - 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.

- Treat with ACE inhibitors such as ramipril to reduce deleterious effects of the positive feedback loop.