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104: Theme 3 - 304 - Renal > The Kidney and its function > Flashcards

The Kidney and its function Flashcards

1
Q

What is the function of the urinary system?

A

Excretion: the removal of organic waste products from body fluids Elimination: The discharge of waste products into the environment

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2
Q

What are the two major layers of the kidney?

A
  • Cortex (outer layer): composed of ~1.25 million nephrons - Medulla (inner layer): pyramids drain into pelvis which drain into the ureters
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3
Q

Name the two types of nephrons that exist

A
  • Cortical Nephrons: 70-80%, located in the cortex, part of the short loop of Henle into the medulla - Jextamedullary Nephron: 20-30%, closer to the medulla, loop of Henle extends deep into the renal pyramids
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4
Q

Label the blood supply of the kidney: Renal artery to Nephron to the renal Vein

A
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5
Q

Label the blood supply of the nephron,

A
  • diagram
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6
Q

Explain the Sympathetic Nerve supply of the Kidney

A

Sympathetic supply: postganglionic fibres from the sympathetic chain and fibres from the coeliac ganglion

  • supplies arteries, afferent and efferent arterioles and granular cells
  • reduces blood supply to kidney during stress
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7
Q

Explain the Parasympathetic Nerve supply of the Kidney

A

Parasympathetic supply: efferent supply from the vagus nerve and the ganglion in the hilum

  • may control the tone of the efferent arterioles
  • may modify glomerular filtration rate (GFR) and renal blood flow (RBF) Maybe??
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8
Q

What happens to endogenous substances drugs that cannot be filtered at the glomerulus

A
  • specialised pumps in the proximal tubule transport the compounds from the plasma into the nephron for excretion
  • there are two pumps: organic acids or drugs and organic bases and drugs
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9
Q

What is Glomerular filtration dependent on?

A
  • blood pressure
  • renal blood flow
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10
Q

What is the pathway for glomerular filtrate in the Bowmans capsule?

A
  • through the pores in the glomerular capillary epithelium
  • the basement membrane of the Bowman’s capsule: including the contractile mesangial cells
  • through the epithelial cells of Bowman’s capsule called podocytes via filtration slits into the capsular space
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11
Q

What are the following forces in relation to Glomerular Filtration?

- PGC

- πBS

- PBS

- πGC

A

- PGC: Glomerular capillary Hydrostatic Pressure

- πBS: Bowman’s space Oncotic Pressure ( plasma protein pressure)

- PBS: Bowman’s space Hydrostatic Pressure

- πGC: Glomerular capillary oncotic Pressure

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12
Q

What does PGC and πBS equal?

A
  • the total pressure out of the glomerulus
  • however, the πBS is almost 0
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13
Q

What does PBS and πGC equal?

A
  • the pressure going into the glomerulus
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14
Q

What is the equation for filtration pressure and how does it work?

A

PGC - (PBS- πGC)

  • πBS = <span>0 so it isn’t included in the equation</span>

<span>- the net filtration is out of the glomerulus at <strong>10mmHg</strong></span>

<span>- this gradually decreases by the glomerular capillary</span>

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15
Q

What is the GFR?

A

Glomerular Filtration rate

  • 125mL/day
  • remains constant even when there is a systematic change in BP
  • this is due to autoregulation of renal blood flow
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16
Q

What are the two hypotheses for Autoregulation of Renal Blood Flow?

A

Myogenic response: (Starling’s Law) change in BP causes arterioles to stretch or constrict to maintain the RBF and in turn GFR

Metabolic response: renal metabolites modulate afferent and efferent arteriolar contraction and dilation. i.e Adenosine, Nitric Oxide

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17
Q

What are the five major stages of urine formation, and where do they occur in the kidney?

A
  1. Filtration of blood in the Glomerulus
  2. Reabsorption of filtrate and Secretion into tubule in the Proximal tubule
  3. Concentration of urine in the Loop of Henle
  4. Modification of urine in the Distal tubule
  5. Final modification of urine in the Collecting Duct
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18
Q

Explain what happens when the FR falls.

A
  • less Na+ enters the proximal tubule
  • the macula densa in the distal tubule senses a change in tubular Na+ levels
  • this stimulates juxtaglomerular cells to release renin into the blood
  • renin release leads to the generation of angiotensin II
  • Ang II is a vasoconstrictor, causing BP to increase
  • increased BP causes filtration pressure to increase and GFR returns to normal
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19
Q

What is reabsorbed in the Proximal tubule and what drives the process

A
  • 60-70% of filtered water, Na+, HCO3-, Cl-, K+ and urea are reabsorbed
  • almost complete reabsorption of glucose, amino acids, a small number of filtered proteins
  • reabsorption is driven by Na+K+ATPase
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20
Q

Describe the action of the Na+K+ATPase pump in the Proximal tubule

A
  • pump is in a 3:2/ Na:K ratio
  • PT cells have alow intracellular Na+ conc.
  • Cl- follows Na+ by facilitated diffusion,
  • phosphate and sulphate are also co-transported with Na+
  • PT has an overall negative charge due to the intracellular proteins
  • water moves out of PT via osmosis following Na+ out into the interstitial space then the Peritubular capillary
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21
Q

What facilitates water reabsorption in the PT?

A
  • PT is very permeable to water
  • Transcellular movement of water occurs via aquaporins

the four main ones

  • AQP-1: abundant in the PT and the descending limb of the LOH
  • AQP-2: abundant in the collecting duct, expression controlled by ADH
  • AQP-3/4: present on the basolateral surface of tubular cells involved with water reabsorption
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22
Q

Explained how glucose is reabsorbed from the PT?

A
  • co-transported from the PT using Sodium-Glucose transporters (SGLT) found on the apical membrane
  • then they are transported into the blood through GLUt channels on the basolateral membrane

in S1: Proximal convoluted tubule

  • SGLT2 channels and Glut 2 channels (90% of glucose absorbed)

in S3: Proximal straight tubule

  • SGLT1 channels and Glut1 channels (10% of glucose absorbed)
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23
Q

How can changing the reabsorption mechanism in the PT treat type II diabetes

A
  • patients excrete more glucose to cause a hypoglycaemic effect

SGLT2 inhibitors

  • Dapagliflozin
  • Canagliflozin
  • Empagliflozin
  • Ipragliflozin
  • Topogliflozin
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24
Q

What is Dapagliflozin?

A
  • A Sodium-Glucose Transport 2 (SGLT2) inhibitor
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25
Q

How are protein reabsorbed in the PT (proximal tubule)?

A
  • reabsorbed by pinocytosis
  • these are vesicles transported into the cell degraded by lysosomes and amino acids returned to the blood
  • there’s only a limited transport capacity
  • therefore proteinuria is a sign of glomerular damage and impending renal failure as there should only a low amount of protein in the filtrate
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26
Q

What do the specialised pumps OAT and MRP do?

A
  • transport compounds that may not be able to be filtered from the plasma into the nephron

OAT: Organic Anion Transporter

MRP: Multi-drug Resistance Protein

alpha-Ketoglutarate is one of the substances OAT3 channels pump into the blood from the PT

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27
Q

What is PAH and what is it’s use in the PT?

A

Para-amino hippurate

  • secreted into the PT from the blood
  • not an endogenous compound so it can be used to measure tubular secretion
  • transported into PT cells from blood with alpha-ketoglutarate or other ci/tri carboxylates
  • It is transported out of the PT cells one exchange for the anion present in the PT lumen
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28
Q

What occurs in the Loop of Henle?

A
  • recovery of fluid and solutes from the glomerular filtrate
  • extraction of water in the descending limb
  • extraction Na+ and Cl- in the ascending limb
  • in the juxtamedullary nephron this is more important as the nephron is longer hence a longer LOH
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29
Q

How is the descending limb of the LOH fit for its purpose?

A
  • cells are flat no active transport channel proteins ( no Na+ or Cl-)
  • Has AQP-1 channels, freely permeable to water
  • passive movement of water via tight junctions
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30
Q

How is the ascending limb of the LOH fir for purpose?

A
  • tubular wall is permeable to water
  • has specialised Na+/K+2Cl- (NKCC2) co-transporters: this is electroneutral as the ratio is 1:1:2
  • Na+, K+ and Cl- is reabsorbed but no water
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31
Q

What is countercurrent multiplication?

A
  • this occurs in the LOH
  • it creates a large osmotic gradient in the medulla allowing the filtrate to vary from isotonic entering the LOH, to hypertonic in the descending limb, then hypotonic in the ascending limb
  • this is facilitated by the NKCC2 cotransporter in the ascending limb
  • it allows passive reabsorption of water from tubular fluid in the descending limb
  • in the ascending limb, ions are being pumped out into the medulla,
  • the medulla becomes hypertonic so water in the descending limb moves into the medulla low
  • this can also be facilitated by the movement of urea into the medulla from the collecting duct
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32
Q

What percentage of filtrate is reabsorbed into the blood from the LOH?

A
  • Water: 15%
  • Na+: 20-30%
  • K+: 20-30%
  • Cl-: 50%
  • HCO3-: 10-20%
  • Ca2+ and Mg2+ : variable
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33
Q

What is the function of the Distal Tubule?

A
  • Na+ and Cl- exchanged for K+ throughout the DT
  • Na+ exchanged for K+ in the late DT and early collecting duct
  • K+ secretion occurs through Principal Cells: these are sensitive to aldosterone
  • this is part of the RAAS
  • Na+ exchanged for H+ in the DT and early collecting duct
  • involves intercalated cell type alpha or beta: these are involved in acid-base regulation
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34
Q

How does the RAAS work in the DT?

A
  • low sodium in the Distal tubule leads to low BP
  • sensed by the macula densa
  • stimulates juxtaglomerular cells which release Renin
  • concerts angiotensinogen to angiotensin I
  • angiotensin converted to angiotensin II using ACE from the lungs
  • increased secretion of aldosterone from the adrenal glands
  • increases NA+ reabsorption from the DT into the peritubular capillary
  • increased H2O reabsorption into peritubular capillary following Na+
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35
Q

What is the action of alpha-intercalated cells

A
  • Secretes acid via H+/Na+ or H+/K+ exchange, involving ATPase or H+ATPase
  • resulting in the reabsorption of HCO3-
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36
Q

What is the action of beta-intercalated cells in the DT?

A
  • secrete HCO3- via Pendrin
  • results in Reabsorption of H+
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37
Q

What is Vasopressin, where is it released from what is its action?

A
  • it is human antidiuretic hormone (ADH)
  • it is released from the posterior pituitary gland, following hypothalamic stimulation
  • has a plasma half-life of 10-15 mins
  • acts on vasopressin V2 receptors on the basal membranes of principal cells in the DT and collecting duct
  • activates AQP2 water channels
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38
Q

What is Diabetes Insipidus?

A
  • lack of ADH causing a water-impermeable collecting duct
  • this leads to large volumes of water being excreted each day
  • treated with synthetic ADH
  • two major presenting forms can be Nephrogenic or Neurogenic

other forms Diposeogenic or Gestational

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39
Q

What is Nephrogenic Diabetes Insipidus and what is its treatment?

A
  • the inability of the kidney to respond to ADH normally

Treatment

  • chlorthalidone (diuretic)
  • Indometacin (anti-inflammatory)
40
Q

What is Neurogenic Diabetes Insipidus and what is its treatment?

A
  • Due to lack of ADH production by the brain

Treatment

  • Desmopressin (ADH analogue)
  • Vasopressin
  • Carbamazepine (anti-convulsive)
41
Q

What is SIADH?

A
  • Syndrome of Inappropriate ADH
  • excessive release ADH : head injury, unwanted effect of drugs (ecstasy)
  • can cause hyponatraemia (low blood Na+ conc.) and possibly fluid overload
42
Q

What is the treatment for SIADH?

A
  • Syndrome of Inappropriate ADH
  • V2 receptor blockers (ADH inhibitors)
    e. g: demeclocycline, Tolvaptan
43
Q

What substances can increase or inhibit ADH?

A

Increase

  • Nicotine
  • Ether
  • Morphine
  • Barbiturates

Inhibit

  • Alcohol
44
Q

What are the 7 groups of patients at risk of developing renal failure?

A
  • Extremes of Age: GFR matures at 4 yrs, decreases after 40 yrs
  • Polypharmacy

- Specific Disease States: diabetes, hypertension, CHF, rheumatoid arthritis, renal disease, recurrent UTI

  • Patients receiving long-term Analgesia: NSAIDs = nephrotoxic
  • Transplant patients
  • Drug therapy: antibiotics, anti-HIV etc
  • Patients undergoing Imaging procedures: radiocontrast used
45
Q

What are the 3 main ways to Monitor Renal Function

A
  • Patients clinical condition:
    • clinical assessment
    • Use of bedside clinical tests
  • Modern imaging techniques
    • macroscopic views of the renal blood flow, filtration and excretory function
  • Biochemical data
    • measurement of renal clearance of various substances i.e creatinine
    • allows evaluation of the ability of the kidney yo handle water and solutes
46
Q

What basic functions should be monitored in the clinical assessment?

A
  • Fluid balance
  • Electrolyte regulation: K+, Na+, Ca2+, PO42-
  • EPO production
  • Vitamin D3
  • Excretion of substances
  • Acid-base balance
47
Q

What are the clinical signs and presenting symptoms of power fluid balance?

A
  • Oedema
  • presenting as breathlessness
48
Q

What are the clinical signs and presenting symptoms of poor EPO production?

A
  • Pallor (check mucous membranes)
  • presenting as fatigue
49
Q

What are the clinical signs and presenting symptoms of poor electrolyte regulation?

A

Abnormal ECG

  • Absent P waves
  • Broad QRS complex
  • Peaked T waves
50
Q

What are the clinical signs and presenting symptoms of low vitamin D3 production?

A
  • Osteomalacia
  • presenting as bone pain
51
Q

What are the clinical signs and presenting symptoms of poor renal excretion?

A
  • raised blood urea and creatinine conc.

presenting with

  • Pruritis (itching)
  • Nausea and vomiting
52
Q

What are the clinical signs and presenting symptoms of a poor acid-base balance?

A
  • Low blood pH and BIcarb levels
  • presenting with deep and rapid respiration
53
Q

What are 4 bedside clinical tests/ data that can be gathered for clinical assessment of renal impairment?

A
  • Weight charts
  • Fluid balance charts
  • The degree Oedema
  • Results of urine dipstick testing: urinalysis for protein, blood and glucose levels
54
Q

Give modern imaging techniques that can/could be used in diagnosing renal impairement

A

Renography

others

  • Gamma camera planar scintigraphy
  • Positron emission tomography (PET)
  • Single protein emission computerised tomography (SPECT)
55
Q

What type of data can you get from biochemical testing to help diagnose renal impairment?

A
  • Plasma or serum creatinine (sCR)
  • Plasma or serum urea
  • Blood urea nitrogen
56
Q

What makes up Plasma?

A
  • serum + clotting factors (i.e fibrinogen)
57
Q

What is creatinine and how is it excreted?

What is its normal plasma range?

A
  • it’s a breakdown product of creatine phosphate in muscle: produced at a constant rate
  • filtered at eh glomerulus, some excretion into the proximal tubule
  • normal plasma range: 40-120µmol/L
58
Q

What causes plasma creatinine to increase?

A
  • large muscle mass/ dietary intake
  • drugs which interfere with analysis: methyldopa, dexamethasone, cephalosporins
  • drugs wich inhibit tubular secretion: cimetidine, trimethoprim, aspirin
  • ketoacidosis (affects analysis)
  • Creatine kinase activity
59
Q

What is the correlation between the severity of the renal failure and the plasma creatinine levels?

A
  • the more severe the renal impairment the higher the plasma creatinine levels
60
Q

What is the normal range of Blood urea nitrogen?

  • what indicates moderate to sever renal failure?
A
  • 2.5-7.5mmol/L
  • >20 mmol/L indicates moderate to sever renal failure
61
Q

What causes BUN- blood urea nitrogen to increase?

A
  • High protein diet
  • Hypercatabolic conditions: severe infections, burns, hyperthyroidism
  • Gastrointestinal bleeding; digested blood is a source of urea
  • Muscle injury
  • Drugs: Corticosteroids (lowers inflammation), Tetracycline (antibiotic)
  • Hypovolaemia
62
Q

What causes decreased plasma creatinine levels?

A
  • Reduced muscle mass (the elderly)
  • Cachexia/ starvation
  • Immobility
  • Pregnancy: increased plasma volume in the mother
  • severe liver disease: liver is also a source of creatinine
63
Q

What causes decreased BUN- blood urea nitrogen levels?

A
  • Malnutrition
  • Liver disease
  • Sickle cell anaemia due to increased GFR
  • SIADH: Syndrome of Inappropriate ADH
64
Q

What is the equation used to measure renal clearance?

A

Cx= Ux x V/Px

Cx= Clearance of X

Ux= COnc. of X in urine

V= Volume of urine formed in a given time

Px= Conc. of X in systemic blood plasma or serum

65
Q

What are the qualities of an ideal marker of kidney function?

A
  • a naturally occurring molecules
  • not metabolised
  • only excreted in the kidney
  • filtered but not absorbed not secretes or reabsorbed by the kidney (Insulins)
66
Q

Define and explain what renal clearance is?

A
  • the volume of plasma completely clearance of a given substance in unite time
  • compares the rate at which the glomeruli filter a substance against the rate at which the kidney excretes that substance via urine
67
Q

What 3 basic functions of the kidney does measurement of Renal clearance give information about?

A
  • Glomerular filtrate (F)
  • Tubular reabsorption (R)
  • Tubular secretion (S)
68
Q

What are some drawbacks of the renal clearance equation?

A
  • have to measure overall nephron function
  • this gives the sum of all transport process occurring along nephrons
  • no information about precise tubular sites or mechanisms of transport
69
Q

Which organic product is best for measuring GFR?

A

Insulin

  • it is filtered in the glomerulus but not secreted in the tubules
70
Q

What are some drawback of using Insulin Clearance to measure GFR?

A
  • Insulin must be administered by IV to get relatively constant plasma or serum levels
  • chemical analysis is technically demanding
  • radiolabeled compounds could be used instead of i.e Vit B or EDTA (these may bind to proteins and distort results)
  • an endogenous substance with insulin-like properties i.e creatinine
71
Q

Why can creatinine clearance be used to give the GFR?

A
  • the Jaffe calorimetry method underestimates creatine conc.
  • this balances out the overestimate from using the Cx equation
  • this makes creatinine clearance ~ insulin clearance
  • it can also be adjusted to body surface area

measured CrCl x 1.73/ BSA

72
Q

How can GFR be estimated without collecting urine samples?

A
  • using the Cockcroft-Gault Formula
    est. GFR (eGFR) = [(140 – Age) x mass (in kilograms)/ plasma creatinine (µmol/L)] x multiplier
  • multiplier = 1.23 men, 1.04 women
73
Q

What is most commonly used in the UK to estimate GFR?

A
  • MDRD (Modification of Diet in Renal Disease) Formula:
  • eGFR = 32788 X plasma creatinine-1.154 X age-0.203 X multiplier
  • mulitplier: 1.21 for black people, 0.742 for non-black women
74
Q

What is PAH para-amino hippuric acid and how can it be used for measuring renal function?

A
  • not usually present in the blood flow
  • when given almost all is cleared from the kidney in one passage, some is filtered in the glomerulus and remainder is secreted by the PT
  • ~10% by-passes tubule, travels from efferent arterioles into peritubular capillaries and then into venous renal blood and is not secreted
  • the uncorrected value of PAH clearance is used and is known as Effective Renal Plasma FLow (ERPF)
75
Q

What is the limit for plasma pH levels before Acidosis results?

A
  • below 7.35
76
Q

What is the limit for plasma pH levels before Alkalosis results?

A

above 7.45

77
Q

What is the consequences of blood pH outside of their homeostatic boundaries?

A

can result in

  • coma
  • cardiac failure
  • circulatory collapse

at pH <6.8 or >8.0 death occurs

78
Q

Give the 3 main types of buffer systems?

A
  • Carbonic/bicarbonate
  • Protein
  • Phosphate
79
Q

How do the lungs and kidneys work in tandem to achieve an acid-base balance?

A
  • lungs excrete a large amount of CO2, which could potentially lead to H+ being produced
  • the kidneys secrete and excrete non-volatile acids produced from metabolism i.e. lactic acid, which the lungs can’t excrete
  • however, kidneys also reabsorbed large amounts of HCO3-, which acts as a buffer
80
Q

How is acidemia controlled in the Proximal Tubules of the kidney?

A
  • increased H+ secretion, through Na+ anti-tranporter
  • Increased HCO3- reabsorption through Na+ cotransporter
81
Q

How is acidemia controlled in the Distal Tubule and the Collecting Duct (Intercalated cells) of the kidney?

A
  • Increased H+ secretion into the tubular fluid
  • Increased HCO3- reabsorption from the tubular fluid
  • HCO3- generation from amino acids, destination occurs
  • HCO3- exchanged with Cl- from the peritubular capillary, forms Sodium Bicarb in peritubular capillary
82
Q

What is the cause and treatment of respiratory acidosis?

A

Cause

  • inadequate ventilation; chronic or acute

Treatment

  • restore ventilation
  • treat underlying dysfunction or disease
  • IV lactate solution (converted to HCO3- buffer in the liver)
83
Q

What is the cause and treatment for metabolic acidosis?

A

Cause

  • all conditions other than respiratory that decreases pH; always chronic

Treatment

  • IV isotonic HCO3-
  • IV lactate solution (converted toHCO3- buffer in the liver); Ringer’s or Hartmann’s solution
84
Q

How can you suffer a loss of H+ ions (may contribute to alkalosis)?

A
  • use of H+ in the metabolism of organic anions
  • loss in vomit
  • loss in urine
  • Hyperventilation
85
Q

What is the cause and treatment of respiratory alkalosis?

A

Cause

  • Hyperventilation: acute or chronic

Treatment

  • treat underlying cause
  • breathe into a paper bag
  • GIve IV Cl- containing solution- increase HCO3- secretion
86
Q

What is the cause and treatment of metabolic alkalosis?

A

Cause

  • all conditions other than respiratory that increase pH; always chronic

Treatment

  • give electrolytes to replace those lost
  • give IV Cl- containing solution (increase HCO3- excretion)
  • treat the underlying condition
87
Q

What physiological factors in the body triggers the release of ADH (vasopressin)?

A
  • Plasma Osmolality
  • Effective Circulating Volume (ECV):
88
Q

For Plasma Osmalality what is the following?

  • Sensors
  • Efferent pathways
  • Effector
  • Affect
A
  • Sensors: Osmoreceptors in the hypothalamus
  • Efferent pathways: ADH, Thirst
  • Effector: Kidney, Brain: drinking behaviour
  • Affect: renal excretion of water, water intake
89
Q

For Effective Circulating Volume, what is the following?

  • Sensors
  • Efferent pathways
  • Effector
  • Affect
A
  • Sensors: Baroreceptors
  • Efferent pathways: ADH, RAAS, ANP, SNS
  • Effector: ST: heart, blood vessels, LT: Kidney
  • Affect: ST: blood pressure, LT: Na+ excretion (decreased in low ECV)
90
Q

Where are the ‘Low pressure’ blood volume receptors amongst the Central vascular sensors?

A
  • Large systemic veins
  • Cardiac atria
  • Pulmonary Vasculature

(very important)

91
Q

Where are the ‘High pressure’ blood volume receptors amongst the Central vascular sensors?

give sites of any other receptors as well

A
  • Carotid Sinus
  • Aortic arch
  • Renal afferent arteriole

(these are less important)

  • there are also sensors in the CNS and liver which are less important
92
Q

ECV= Effective circulating volume

Explain the effect of a decreased ECV and the RAAS

A

Decreased ECV stimulates renin release via:

  • decreased renal perfusion pressure detected in the afferent arteriole (the renal baroreceptor)
  • decreased Na+ concentration in distal tubule detected by the macula densa cells
  • decreased systemic BP also triggers the effect of the SNS supplying the JGA (where renin is released)
  • this leads to increased Na+ reabsorption by the distal tubule
93
Q

What are the important actions of Angiotensin II?

A

All actions of AngII are designed to increase ECV

  1. Enhances tubular Na+ transport in the kidney
  2. Stimulation of aldosterone release from adrenal cortex: more Na+ and water reabsorbed from DT and CD
  3. Acts on the hypothalamus to stimulate thirst and ADH release into circulation
  4. Vasoconstriction of renal and other systemic vessels: increased systemic BP
  5. Longe term: AngII causes renal cells to hypertrophy: more protein synthesis of Na+ transporters and channels
94
Q

What are the important actions of Aldosterone?

A

All actions of aldosterone are designed to increase ECV

  • Stimulates Na+ reabsorption in the DT and CD
  • exerts indirect negative feedback on the RAAS by increasing ECV and by lowering plasma K+ concentrations
  • Important in conserving Na+ and water, but also important in preventing large variation in plasma K+ levels (by causing its excretion out of the kidney)
95
Q

What are the 3/4 volume regulation pathways involving the ECV?

A

RAAS

  • detected by renal baroreceptors and renal Na+ sensors -> activation of the RAAS -> Aldosterone and AngII action

ANS

  • detected by peripheral baroreceptor -> signals to the hypothalamus in the brain -> activation of ANS -> direct effects on renal thermodynamics, activation of the RAAS

ADH

  • detected by peripheral baroreceptor -> signals to the hypothalamus in the brain -> release ADH
  • decreased ECV= increased plasma osmolality -> detected by osmoreceptors in the hypothalamus -> release ADH into circulation
96
Q

Describe the action of Atrial Natriuretic Peptide (ANP)

A

Actions of ANP are all designed to lower ECV

  • Atrial myocytes synthesize and store ANP
  • ­ECV causes atrial stretch which leads to ANP released into circulation
  • ANP promotes natriuresis: (­ Na+ excretion from the kidney)
  • Also causes renal vasodilatation -> increased blood flow -> increase in GFR -> more Na+ excreted
  • More Na+ reaches the macula densa so renin release by JGA is reduced – reduces the effects of AngII
  • Overall effect: inhibits action of Renin and opposes effects of AngII

104: Theme 3 - 304 - Renal (5 decks)

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