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Test 4: A&P
Terms in this set (81)
What is reabsorption?
the process of moving substances in the filtrate from the lumen of the tubule back into the blood flowing through peritubular capillaries
Where does most reabsorption occur?
proximal convoluted tubule (PCT)
In which other regions of the nephron does reabsorption occur that is hormonally regulated?
distal convoluted tubule and collected duct
- water and ions are hormonally controlled
What substances are reabsorbed?
100% Amino Acids
~ 50% of urea is reabsorbed but secreted back into the filtrate
What are passive and active reabsorption?
Passive reabsorption occurs on a concentration gradient with no energy
Active reabsorption occurs if there is no concentration gradient and therefore energy input is required.
What is transcellular reabsorption?
- solute enters the apical membrane of tubule cells
- travels through the cytosol of tubule cells
- exits basolateral membrane of tubule cells
- enters the blood through the endothelium
What is paracellular reabsorption?
BETWEEN TUBULE CELLS
- movement through leaky tight junctions, particularly in the proximal convoluted tubule
- movement through the interstitial fluid into the capillary
How is sodium transported across the tubule epithelium in reabsorption? (basolateral vs. apical membrane)
- almost all transcellular transport
- transported across the basolateral membrane and apical membrane
- primary active transport, Na+/K+ ATPase pumps Na+ out
- Then the flow of water sweeps Na+ into the capillaries
* low hydrostatic pressure and high osmotic pressure in capillary here so water flows in
- enters tubule cell at the apical surface via secondary active transport (cotransport) or via facilitated diffusion through carriers and channels
- this happens because the pump maintains the intracellular Na+ at low levels and the K+ pumped into the tubule cells immediately diffuses out via leakage channels leaving a negative charge inside the cells
How does water move (is reabsorbed) secondary to Na+ movement?
movement of Na+ and other solutes creates an osmotic gradient for water
How are glucose, amino acids and other organic nutrients moved (reabsorbed) secondary to the Na+ gradient? (diagram in my slides and figure 19.8 will be helpful)
Na+ reabsorption by primary active transport provides energy and means for reabsorbing almost every other substance
Organic nutrients are reabsorbed by secondary active transport and are co-transported with Na+
How do fat soluble substances and other ions move (are reabsorbed) passively, secondary to the Na+ gradient and water movement?
fat soluble substances and some ions will follow water into peritubular capillaries down their concentration gradients
- for this reason lipid-soluble drugs and environmental pollutants are reabsorbed even though it is not desirable
How does the movement of Na+ help drive movement (reabsorption) of negatively charged ions like Cl-?
Active movement of Na+ establishes an electrical gradient that promotes passive reabsorption of negatively charged ions like Cl- to maintain neutral membrane potential
How is urea reabsorbed?
ion movement drives the water movement, when water moves back into the capillaries there is less in the tubule lumen, urea concentration becomes higher in the lumen and can move out of the lumen into the interstitial space on a gradient
- facilitated diffusion in response to concentration gradient in the deep medulla region; recycles and contributes to medullary osmotic gradient
What is the transport maximum? What determines the transport maximum of a substance?
the max rate of transport when all carriers are occupied by the substrate (saturation point)
- reflects the number of carriers in renal tubules that are available
Ex. like a moving sidewalk and door
What is saturation?
occurs when carriers for a solute are saturated, the excess that is not reabsorbed is excreted in urine
ex. hyperglycemia leads to high blood glucose levels that exceed Tm and glucose spills over into the urine
What is secretion? What does it depend on? What are some of the key substances that are secreted?
movement of substances from the plasma or extracellular fluid into the tubules
DEPENDS ON: transport systems to get substances across membranes (usually involves movement against gradients so it requires energy)
Key substances secreted:
- K+, and H+
- proximal convoluted and some in the distal and collecting ducts
We used OATs (organic ion transporters) as an example of secretion by tertiary active transport. How did that work? What were the key take home messages from this example that I noted in class and on the slide?
Mechanisms of Organic anion transport
1. Na+/K+ pump maintains low intracellular Na+ (active)
2. NaDC transporter moves dicarboxylate into the cell using Na gradient
3. OAT uses dicarboxylate gradient to move OA inside cell
4. OA moves into the tubule via unidentified transporter
TAKE HOME MESSAGE:
- two steps removed from ATP input, two gradients used
to secrete an unwanted substance in exchange for reabsorbing a wanted substance
What is excretion?
excretion= filtration- reabsorption + secretion
- basically at the end of all the processing through the corpuscle and tubules, what's left to leave the body in urine
What are the factors that determine excretion rate?
- state of the body
- filtration rate of substance
- whether the substance is reabsorbed, secreted or both
the sequence of processes in which the kidney deals with a given substance
- can be determined by the renal clearance
ex. if clearance is less that 125ml/min then renal handling is that the substance was absorbed
is the rate at which a solute disappears from the body by excretion or metabolism
- can be calculated indirectly by how much of a substance is being excreted over how much is in the plasma
How are inulin and creatinine used to determine renal clearance?
inulin, a plant polysaccharide, is the standard used
- filtered but neither reabsorbed nor secreted by the kidneys
Sometimes creatine is used (not as good as inulin but close)
If C< 125 ml/min
substance is reabsorbed
If C= 0
substance was completely reabsorbed or not filtered at all
if C=125 ml/min
no net reabsorption or secretion
If C>125 ml/min
substance was secreted (most drug metabolites like penecillin)
What is micturition? What is the path that a drop of urine would follow from the collecting ducts to outside the body?
the act of emptying the bladder (urination)
- collecting ducts dump urine into the renal pelvis, which merges to the ureter
- ureter carries urine to the bladder where it is stored until released from the body
What are the two sphincters in the urethra that help control urination?
1. internal sphincter
- involuntary (smooth muscle) at bladder-urethra junction
- contracts to open
2. external sphincter
- voluntary (skeletal) muscle surrounding urethra as it passes through pelvic floor
How do the sphincters work? What triggers them? Can you describe the urination reflex? (figure 19.15, and described in last couple slides)
Simple spinal reflex: (can be overridden in adult brains)
- stretch receptors in bladder walls send signals to the spinal cord
- parasympathetic fibers to induce bladder smooth muscle contraction
- somatic neurons to external sphincter are inhibited
What do we mean when we say water and ion homeostasis? Why do we care? How does the concept of mass balance apply?
maintaining water and salt balance in the body
- Mass balance: matching intake with loss and the systems that regulate that
- our body is in constant flux with taking on and losing fluid and electrolytes
What are the physiological mechanisms through which water and ions are lost or excreted?
We consume water and and ions
We lose water and ions via kidneys, feces, exhalation
What are the behavioral mechanisms that drive the intake of new water and salt?
- Thirst drive
- salt appetite
What are the three systems that act to maintain fluid and electrolyte homeostasis, which act faster, which are slower?
Respiratory, cardiovascular, and urinary system
Respiratory and cardiovascular system
- rapid responses, under neutral control
- slow responses; under mostly endocrine/ neuroendocrine control
How much water do we take on and lose each day?
Law of mass balance
2.5 L in 2.5 L out
What are the mechanisms of intake/production of water, what are the mechanisms of excretion/loss?
- 2 L ingested in food and drink
- aerobic metabolism
* Glucose+ O2= CO2 + H2O
* About another 0.3 L per day
- 1.5 L in urine
- small amount in feces
- insensible water loss (sweating and exhalation of water) 900mL
Can you describe the kidneys general role in regulating water loss? Why is it that kidneys can only regulate water balance up to a point by regulating water excretion?
only water loss or retention in urine is regulated for maintaining water balance
- can offset the excessive loss from excessive sweating, diarrhea, etc.
- pathological water loss can decrease ECF and plasma volume, affecting BP
- excessive sweating can affect osmolarity if it is hypoosmotic and results in increased solute concentrations in the body
How does urine concentration reflect the water situation in the body? Think about dilute or concentrated urine.
---> when we need to get rid of more fluid urine is dilute (High volume, low Osm)
----> When we need to conserve fluid, urine is concentrated (low volume, high osm)
Walk through the renal medulla and making concentrated versus dilute urine. You'll want to understand the increased concentration of the interstitial space in the medulla and how it can be used to make concentrated or dilute urine. What is the role of aquaporins? Walk through figure 20.4 in your text
- Occurs through modulation of water and Na+ reabsorption in the tubules and collecting ducts
- To make more dilute urine the tubules reabsorb more solute and not let water follow
- If urine needs to be more concentrated the tubules most reabsorb more water but leave solutes in the filtrate
- the interstitial fluid in the space surrounding the tubules is more concentrated than the filtrate
- make the tubule cells more or less permeable to water depending on whether you need to reabsorb it or not -----> AQUAPORINS
- medullary interstitial osmolarity allows urine to be concentrated
* in the renal cortex reabsorption is isosmotic
* fluid in the descending loop of Henle loses water by osmosis to the medulla (but not the solute)
* cells in the thick portion of the ascending limb of the loop are impermeable to water but actively transport Na+ out of the lumen into the medulla
* medullary interstitial osmolarity allows urine to be concentrated
- distal nephron is permeable to water so the filtrate becomes concentrated
- collecting duct can reabsorb additional solute, filtrate can become even more dilute
How does vasopressin (ADH) regulate the concentration of urine? What does it do in the distal tubules and collecting ducts?
stimulates epithelial cells in the collecting ducts to insert aquaporins into the membrane
- more aquaporins= more water absorption
How is ADH release from the pituitary gland stimulated? What are the stimuli, where are the receptors?
stimulated by changes in plasma osmolarity and blood pressure
- increased plasma osmolarity activated osmoreceptors in the hypothalamus
Low Osm or High BP: no signals, no ADH
High Osm or Low BP: receptors are stimulated and send signals for vasopressin release from the pituitary
What is the Counter current exchange system? Multiplier? Exchanger?
vasa recta and nephron flow in opposite directions
- regions of the loop of Henle are selectively permeable to different substances and flow is down into the medulla then back up
- the filtrate flows down the descending limb which is only permeable to water
- when filtrate round the bottom of the loop and starts back up the ascending side, the epithelium of the tube changes (actively transports out Na+, K+, Cl-)
- urea then contributes to medullary interstitium concentration
RESULT: a dilute filtrate, but hyperosmotic interstitial space that increases in concentration deeper into the medulla
How does the different permeability of the limbs of the loop of Henle contribute to the countercurrent multiplier?
How does filtrate concentration change as it flows through the loop?
How does the concentration of the renal medulla change from its cortical side to its deeper regions?
Know that urea plays an important role in the medullary osmolarity. How does the vasa recta contribute to the countercurrent multiplier?
a lot of structures in one space
filtrate the descending limb is only permeable to water making the filtrate more and more concentrated
then on the ascending limb, there is a concentration gradient for ions to flow out via ion transporters
• Sodium balance is important. Contrast sodium balance to potassium, wherewith sodium we only modulate reabsorption and with potassium, we modulate both reabsorption and potassium.
o Definitely understand why high ECF is a problem for cells, and this is part of why we care about modulating sodium and potassium.
What are the two responses to excess NaCl intake that raises ECF osmolarity?
vasopressin release and thirst
What is the effect of vasopressin/ADH? What is the outcome of increased thirst?
increased aquaporins in collecting duct to increase water reabsorption and increase thirst increase BP and blood volume
How is sodium excreted? How is sodium excretion regulated?
sodium excretion only regulated in the kidneys
hormonally regulated in distal tubule and collecting duct
secondarily related to BP and blood volume
What is aldosterone, where is it produced, what is its effect on sodium reabsorption? What are the slow and fast responses it elicits, and in what cells do those responses occur?
"salt-retaining hormone" which promotes the retention of Na+ by the kidneys. na+ retention promotes water retention, which promotes a higher blood volume and pressure
produced in the adrenal cortex
fast: activating already present channels
slow: transcription of new channels
What are the two primary stimuli for aldosterone release? How do each of those stimuli stimulate aldosterone release?
1. intracellular K+ detected in adrenal cortex
2. Low BP
renin stimulates aldosterone pathway
What is the RAAS? What cell types are involved?
The renin-angiotensin Pathway:
- juxtaglomerular cells (granular cells) secrete the enzyme renin if blood pressure decreases
- renin converts angiotensinogen to angiotensin I (from the liver)
- ACE converts angiotensin I to angiotensin II (in the lungs)
- angiotensin II increases blood pressure through these pathways:
1. increases vasopressin secretion
2. stimulates thirst
3. a very potent vasoconstrictor
4 increases SNS activity
5. increases proximal tubule Na+ reabsorption
How is the RAAS activated?
1. granular cells are sensitive to blood pressure
2. sympathetic stimulation from cardiovascular center
3. paracrine feedback from macula densa cells
------> ALL stimulate adrenal cortex to produce aldosterone
What are the natriuretic peptides? What is their effect? Where are they produced?
hormones that cause sodium and water loss (antagonists to RAAS)
1. atrial natriuretic peptide
2. brain natriuretic peptide
atrial natriuretic peptide
- produced by cells in the atrial myocardium
- myocardial stretch (Increase BP) triggers release
- Enhances Na+ and water excretion through multiple mechanisms:
* increases GFR
* decreases collecting duct Na+ reabsorption
* suppresses effects of renin, aldosterone, and vasopressin
Brain Natriuretic Peptide (BNP)
- produced in the central brain neurons but also the ventricular myocardium
- used as a marker to estimate heart failure because production increases with pathological ventricular dilation and hypertrophy
Why is potassium balance more complicated than sodium balance?
potassium is both secreted and reabsorbed
- ECF concentrations need to be kept in a very narrow range
excessive potassium in the blood
- decreases the K+ gradient across cell membranes
- resting membrane potential becomes less negative
- cardiac arrhythmias (neurons become less excitable)
deficient potassium in the blood
Where do potassium reabsorption and secretion occur in the kidney tubules? What are the common disturbances for potassium levels? Know that aldosterone is complicated because it combines sodium and potassium movement, and how it does that.
- reabsorbed in the proximal tubule and ascending limb
- secreted in the collecting ducts
- excretion is balanced with the intake
- aldosterone increases K+ excretion
What are the only ways we increase body water and sodium?
How are thirst and salt appetite stimulated? What is the brain region important in these responses?
hypothalamus for thirst
- due to changes in body osmolarity
hypothalamus for salt
In the integrated control of salt and water balance, what are the two major systems that contribute to control? What are the two general things that each respond to?
cardiovascular and kidney
- blood pressure
Be able to explain how osmolarity of body fluid and volume of body fluid can change independently
o There are 3 states for each volume and osmolarity: normal, decreased, increased
o That means that I added to normal, there are 8 other combinations of states you can have for your body fluid (increased volume with normal osmolarity, etc..)
CHART on study guide
Table 20.1 seems like a lot, but its really a summary of everything we have talked about for how the body responds to different changes in body fluid volume, blood pressure and osmolarity. o Id review this table
What were the 3 things the overall response needs to achieve during severe dehydration?
What are the 4 components of the response?
How does each function? This is Figure 20.13, I know its daunting but its all stuff we've covered, now just put into 1 diagram o What is the net result of the response if it is successful?
Needs to achieve:
1. conserve fluid to prevent additional loss
2. trigger cardiovascular responses to maintain blood pressure
3. stimulate thirst to restore fluid volume and osmolarity
What is acid/base balance?
Essentially a measure of H+ concentration
- expressed as pH
What is normal body pH? Is pH in all body fluids the same?
Normal body pH is 7.4 (7.38-7.42)
no stomach gastric juice can have a pH of 2 and urine can range from 4.5 to 8.5
What is abnormal pH? What are acidosis and alkalosis?
below or above 7.4
acidosis: low body pH
- neurons become less excitable
- depressed nervous system activity
alkalosis: high body pH
- neurons become hyperexcitable
- increased and uncontrolled nervous system activity
* tied to K+ balance as kidney moves H+ and K+ in antiport (if pH is low, kidneys excrete H+ but retain K+ and vice versa)
What are the major sources of acid input into the system? External and metabolic.
- In food and byproducts of metabolic pathways
- substances that can lose/ donate H+ to body fluids
* organic acids (amino acids, fatty acids, etc)
- normally balanced with secretion; in extreme cases can cause crisis:
* ketoacidosis occurs in diabetics due to abnormal metabolism of fats and amino acids where ketoacids, which are very strong acids are created
What is a buffer?
a substance that minimizes changes in pH
What are the 3 major buffering systems in our body and how fast can each respond to a disruption in pH homeostasis?
1. chemical buffers (first line of defense)
2. ventilation (rapid, reflex controlled)
3. renal regulation of H+ and bicarbonate (slow, but very effective)
What are chemical buffers? What are the major chemical buffers in our body?
Chemicals that combine with or release H+
Intracellular buffers: include proteins, HPO42- (phosphate ions), hemoglobin
Extracellular buffers: most important is bicarbonate in the plasma
- some H+ binds directly to hemoglobin, bicarbonate from the carbonic anhydrase reaction goes into the plasma and can buffer more
What is ventilation buffering? How can ventilation be changed to buffer CO2?
Extra CO2 produced by bicarbonate buffering can be exhaled
- respiratory compensation: increase in metabolic acid production os "compensated for" through buffering and subsequent removal of increased CO2 by increased ventilation
How can altered ventilation cause disturbances in pH? Use the bicarbonate equation as a visual. Also Figure20.15
- hypoventilation increases PCO2, shifts the equation to the right and causes acidosis
- hyperventilation decreases PCO2, shifts equation left and can cause alkalosis by decreasing H+
the two ways the kidney can act in renal buffering? What would the kidney do in a state of acidosis? Alkalosis?
1. excrete or reabsorb more H+ (direct mechanism)
2. Excrete or reabsorb more bicarbonate (indirect mechanism)
- directly secrete more H+
- ammonia from amino acid break down and phosphate ions buffer some H+ ions in the urine ot allow even more to be secreted
- kidneys can make new bicarbonate which is reabsorbed
- reabsorb more H+
- excrete bicarbonate and reabsorb H+
What are the 4 kidney epithelial transporters involved in acid base balance? What does each do?
1. apical Na+-H+ exchanger (NHE)
- active transporter brings Na+ into cell to move H+ against its gradient
2. Basolateral Na+-HCO3- symporter
- moves Na+ and HCO3- out of epithelial cell into interstitial fluid
- moves H+ into urine in exchange for reabsorbed K+
- can lead to K+ imbalances
4. Na+-NH4+ antiporter
- moves NH4+ (ammonium) from cell to nephron lumen in exchange for Na+
How is bicarbonate reabsorbed in the proximal tubule? Figure 20.17
- there is no direct transporter for bicarbonate, reabsorbed indirectly
Proximal tubule can reabsorb in 2 ways:
1. converts filtered HCO3- into CO2 then back into HCO3-
- net reabsorption of Na+ and HCO3-
2. Metabolism of glutamine (amino acid)
- Net reabsorption Na+ and HCO3-
How is acid secreted in the distal tubule?
Intercalated cells (type A)
- have high intracellular concentrations of carbonic anhydrase
- can rapidly convert CO2 and H2O to H+ and bicarbonate
- H+ is pumped out by ATPase pumps
What are the two types of intercalated cells and what do they do?
- Type A secrete H+ and reabsorb bicarbonate
- Type B secrete bicarbonate and reabsorb H+
when H+ input exceeds H+ excretion
- dietary and metabolic sources
- produces more CO2 and uses up HCO3- buffer
- lactate in anaerobic metabolism
- ketone production
- loss of HCO3- due to diarrhea (most common)
- respiration adjusts fairy quickly
- renal compensation also occurs (excrete H+ and reabsorb HCO3-)
- excessive vomiting of stomach acid (HCl)
- excessive ingestion of bicarbonate (antacids)
reduces H+ and increases HCO3- (plasma CO2 decreases)
- ventilation compensation is rapid
* hypoventilation retains CO2
- Renal compensation secretes HCO3- and reabsorbs H+
Alveolar hypoventilation resulting in CO2 retention
- elevates plasma CO2
- more CO2 pushes equation to the right so decreased pH with elevated HCO3-
- drugs that depress ventilation
- increased airway resistance
- impaired gas exchange (fibrosis or pneumonia)
- muscle weakness (inspiratory muscles)
- COPD (emphysema)- most common cause
Compensation: Renal only way
- excrete H+ and reabsorb HCO3-
- try to decrease H+ ions and increase buffering capacity
results from hyperventilation
- artificial ventilation
- hysterical hyperventilation (paper bag breathing)
alveolar ventilation increases but not metabolic CO2 production
- plasma CO2 falls
- plasma H+ and HCO3- decrease
Only compensation is renal
- HCO3- secretion and H+ reabosorption
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