Physiology- Renal III Flashcards
Extracellular fluid Na conc and osmolarity are regulated by
Amt of extracellular water
Osmolarity determined by
Amt of solute/vol ECF
Total body water controlled by
Fluid intake
Renal excretion of water
As water levels in body increase, what happens to osmolarity
Decreases
Antidiuretic hormone AKA
Vasopressin
Role of antidiuretic hormone
Regulates plasma osmolarity and sodium conc by altering renal excretion of water independently of rate of solute excretion
Antidiuretic hormone feedback loop
Increased osmolarity sensed by osmoreceptors in hypothalamus–> posterior pituitary secretes ADH–> increases permeability of distal tubule and collecting ducts to water
What parts of the kidney does ADH act on?
Distal tubule
collecting duct
Tonicity of glomerular filtrate compared to plasma
Isotonic (same osmolarity)
Proportion of solutes and water absorbed in proximal tubule
Equal proportions—> little change in osmolarity
How is water absorbed in descending loop of henle
Osmosis
Obligatory urine volume
Amount of urine necessary to be excreted per day to to rid body of metabolic waste products
In normal person = .5 L/day
What is obligatory urine volume dictated by?
Maximal concentrating ability of kidney
Why you shouldn’t drink sea water
1 L sea water in = 1.5 L water excreted
Leads to dehydration
Requirements to excrete a concentrated urine
High level of ADH
high osmolarity of renal medullary interstitial fluid
-countercurrent mechanism
Major factors contributing to hyperosmotic renal medullary interstitium
- Active transport of Na ions and co-transport of K Cl and other ions out of thick ascending loop of henle into medullary interstitium
- Active transport of ions from collecting ducts into medullary interstitium
- Facilitated diffusion of urea from inner medullary collecting ducts into medullary interstitium
- Diffusion of less water than reabsorption of solutes from medullary interstitium
Countercurrent multiplier
Repetitive reabsorption of NaCl by thick ascending limb of loop of henle and continued inflow of new NaCl from proximal tubules into loop of henle
How cortical collecting ducts play a role in concentrating urine
If ADH levels are high, cortical collecting ducts become permeable to water
-large amts of water get reabsorbed from tubule into cortex interstitium, where it is swept away by capillaries
Why is water reabsorbed into cortex from collecting ducts instead of renal medulla?
To preserve high medullary interstitial osmolarity
Role medullary collecting ducts play in concentration of urine
Wen ADH present, water gets further reabsorbed in interstitium and carried away from vasa recta
-urea is reabsorbed from medullary collecting duct into medullary interstitium and is “recycled”
2 features of renal medullary blood flow that contribute to preservation of hyperosmolarity of renal medulla
Low medullary blood flow
Vasa recta serve as countercurrent exchangers
Level plasma osmolarity is maintained at
280-295
What level is plasma osmolarity at when thirst is sensed
294 mOsm/L
What level does osmolarity have to raise by for ADH release to be stimulated
1%
Disturbances in osmolarity are reflected by
Alterations in serum Na concentrations; hyper/hyponatremia
ADH secretion is stimulated by
Hyperosmolarity
Volume depletion
What is hyperosmolarity sensed by
Hypothalamic osmoreceptors
What is volume depletion sensed by
Carotid sinus baroreceptors
Extracellular fluid volume determined mainly by
Balance between intake and output of water and NaCl
If ingestion of NaCl is greater than excretion of NaCl, what will happen to ECF volume?
Will increase
If excretion of NaCl is greater than ingestion of NaCl, what happens to ECF volume?
Decreases
Sensors that control ECF volume
Vascular low pressure volume sensors*
Vascular high pressure volume sensors*
CNS
hepatic system
Where vascular low pressure volume sensors are located
Walls of cardiac atria
Right ventricle
Pulmonary vessels
How much of a change in blood volume is required to evoke a response from vascular low pressure volume sensors
5-10% change in blood volume and pressure
What happens in response to vascular low pressure volume sensors sending signals to brainstem
Modulation of sympathetic nerve outflow and ADH secretion
- decrease in filling increases sympathetic nerve activity and stimulates ADH
- dissension of structures decreases sympathetic nerve activity
Where are vascular high pressure volume sensors located
Arterial side of circularity system
Wall of aortic arch
Carotid sinus
Afferent arterioles in kidney
How much of a change in blood pressure is required for vascular high pressure volume receptors in aortic arch and carotid sinus to send signals to brainstem
5-10%
Decrease in BP sensed by vascular high pressure volume sensors causes what?
Increases sympathetic nerve activity and ADH secretion
Increase in BP sensed by vascular high pressure volume sensors causes
Decrease in sympathetic nerve activity
When vascular high pressure volume sensors sense a change in volume at afferent arteriole of kidney, what structure responds to these changes
Juxtaglomerular apparatus
Juxtaglomerular apparatus response to reduced perfusion pressure in afferent arteriole
Release of renin
Juxtaglomerular apparatus response when an increased perfusion pressure is sensed
Suppression of renin release
Volume sensor signals
Sympathetic nerves
Renin-angiotensin-aldosterone system
Natriuretic peptides
Antidiuretic hormone
With ECF depletion, stimulation of renal sympathetic nerve activity leads to
Constriction of afferent and efferent arterioles
Renin secretion stimulated by granular cells
NaCl reabsorption along nephron stimulated directly
What is the net effect of renal sympathetic activity
Decrease excretion of NaCl
Restore ECF volume to normal
Renin secretion stimulated by
Reduced perfusion pressure
Sympathetic nerve activity
Reduced delivery of NaCl to macula densa
Functions of angiotensin II
Stimulation of aldosterone secretion by adrenal cortex
Arteriolar vasoconstriction, increasing BP
stimulation of ADH secretion and thirst
Increase NaCl reabsorption by proximal tubule, thick ascending loop of henle, distal tubule, and collecting duct
Stimulates secretion of aldosterone
Natriuretic peptides
ANP and BNP are secreted when heart dilates to relax vascular smooth muscle and promote excretion of NaCl and water by kidneys
Hi and low pressure volume sensors send signals to kidneys to increase excretion of NaCl and water by:
Decreasing sympathetic nerve activity Releasing natriuretic peptides Inhibit ADH secretion Decrease renin secretion Decrease aldosterone secretion
General responses of nephrons to the need for volume sensors to want to get rid of sodium and water
GFR increases
Reabsorption decreases in proximal tubule and loop of henle
Sodium reabsorption decreases in distal tubule and collecting duct
Extracellular volume depletion cause kidneys to
Reduce excretion of NaCl and water
Reduced excretion of NaCl and water is done by
Increasing sympathetic nerve activity
Increased secretion of renin
Decreasing natriuretic peptides
Increased secretion of ADH
The kidneys effort to reduce excretion of NaCl and water results in
Decreased GFR
Increased Na reabsorption by proximal tubule and loop of henle
Increased Na reabsorption by distal tubule and collecting duct
Acidemia
Fall in pH (more acidic)
Alkalemia
Rise in pH (more basic)
Most metabolic processes in the body result in the production of
Acid
Largest source of acid from within the body
Catabolism and oxidation of glucose and fatty acids…ultimately CO2+H2O= carbonic acid
What gets rid of volatile acid production
Pulmonary ventilation
Nonvolatile acids formed primarily from
Metabolism of sulfur-containing amino acids
What gets rid of nonvolatile acids
Excretion of H ions thru kidney
H ion conc determined by
Ratio of PCO2 and bicarbonate concentration
3 primary systems to prevent acidosis or alkalosis
- Chemical acid-base buffer systems of body fluids
- Respiratory center
- Kidneys
Chemical acid-base buffer systems of body fluids
Bicarbonate and phosphate buffer systems
Proteins as infra cellular buffers
How respiratory center prevents acidosis/alkalosis
Removal of CO2 and therefore bicarbonate from ECF
How kidneys prevent acidosis/alkalosis
Excrete either acidic or alkaline urine
Body produces how much nonvolatile acid/day?
~80 mEq
Reabsorption of bicarbonate and secretion of H are accomplished through process of
H secretion by tubules
-bicarbonate must combine with H to form H2CO3 before it can be reabsorbed
3 mechanisms used by kidneys to regulate ECF H conc
Secretion of H
Reabsorption of filtered bicarbonate
Production of new bicarbonate
H ion secretion and bicarbonate reabsorption occur in all parts of tubules except
Descending ans ascending thin limbs of loop of henle
What must happen for each bicarbonate to be absorbed
One H must be secreted
How H is secreted in proximal tubules, thick segment of ascending loop of henle, and early distal tubule
Secondary active secretion of H is coupled with Na transport
How intercalated cells of late distal and collecting tubules secrete H
Active transport
Phosphate buffer system
Phosphates are ultimately responsible for holding H+’s in urine so that H+’s can be expelled from the body in urine. This also allows HCO3- to be reabsorbed from the kidney back into the body, without H+ following the HCO3- back into the body.
Ammonia buffer system
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