Regulation of Extracellular Fluid Osmolarity and Sodium Concentration Flashcards
Which hormone is a major determining factor in urine concentration?
ADH
Increase in OSMOLARITY in the body
- INCREASE ADH
- INCREASE water permeability
- large REABSORPTION of water
- INCREASED concentration of urine
- no marked change in excretion of solutes
Osmolarity in proximal tubule
Stays ISOTONIC
Osmolarity in loop of Henle
-enters loops being ISOTONIC
**water is reabsorped by OSMOSIS in the DESCENDING segment of the loop of Henle
- thin and think ascending segments are NOT permeable to water!!!
- solutes are ACTIVELY transported out (THICK)
- tubular fluid becomes more DILUTE as it travels up ascending segments
-leaves loop of Henle as a HYPOTONIC solution
T/F: renal medulla interstitial fluid is very HYPERTONIC
True
-tubular fluid becomes more concentrated as it travels into the medulla
Osmolarity in the distal tubule and collecting ducts
- enters being DILUTE
- later parts:
- additional reabsorption of sodium
- absence of ADH = dilute urine excreted
- presence of ADH = concentrated urine excreted
Urine Specific Gravity
- used as a measurement in clinical settings to assess the concentration of urine
1) high concentration = high specific gravity
2) low concentration = low specific gravity
Basic requirements for forming a concentrated urine
1) HIGH level of ADH
2) HIGH osmolarity in the medulla tissue
How do we create a hyperosmotic renal medullary interstitial fluid?
- COUNTERCURRENT MECHANISM
- juxtamedullary nephrons
- vasa recta
- collecting ducts
- molarity of the renal medullary interstitial fluid
What is the osmolarity around the papilla of the renal pyramids?
~1200mOsm/L
Countercurrent multiplier
the repetitive reabsorption of NaCl by the THICK ASCENDING loop of Henle and continued inflow of new Na+ from the PROXIMAL TUBULE into the loop of Henle
Vasa Recta and urine concentration
- Countercurrent exchangers
- minimizes washout of solutes from the interstitium
- preserve the high solute concentration in the renal medulla
A high concentration of UREA is found in the…
inner medullary collecting ducts
-diffusion of urea into the renal medulla (facilitated by urea transporters)
Thirst
when sodium content increases 2mEq/L above normal there is a desire to ingest fluid
**the THRESHOLD FOR DRINKING
Thirst center
- an area along the anteroventral wall of the THIRD ventricle that promotes ADH release also stimulates thirst
- anterolateral in the PREOPTIC NEURONS
Factors that increase thirst
- INC plasma osmolarity
- DEC blood volume
- DEC blood pressure
- INC angiotensin II
- a dry mouth
Factors that decrease thirst
- DEC plasma osmolarity
- INC blood volume
- INC blood pressure
- DEC angiotensin II
- gastric distension
Extracellular fluid volume (ECV)
- determined by intake and output of fluid and sodium
- usually dependent on person’s HABITS
Homeostatic state of ECV
- must excrete almost the same amount of sodium that you take in (w/in a few days)
- not much change in extracellular fluid
- ADH
- osmolality and sodium concentration are maintained
What happens if ECV can not maintain a steady balance?
- change in BP
- change in circulating hormones
- change in SNS
Pressure diauresis
increased blood pressure raising urinary volume excretion
Pressure natriuresis
the raise in sodium excretion that occurs with elevated blood pressure
T/F: pressure diauresis and pressure natriuresis occur concurrently
True
As long as the pressure diauresis mechanism is working the body will be able to handle an increase in fluid and salt intake with LITTLE change to:
- blood volume
- ECF volume
- cardiac output
- arterial pressure
What circumstances would change the fact that ECF volume and blood volume are controlled together?
- INC capillary hydrostatic pressure
- DEC plasma colloid osmotic pressure
- INC permeability of the capillaries
- obstruction of lymphatic vessels
T/F: an inhibition of sympathetic activity may help to rapidly eliminate excess fluid and sodium when large amounts are consumed
True
What stimulates SNS activity on the kidneys?
an extensive decrease in blood volume (i.e., hemorrhage)
- signals kidneys to HOLD ON TO salt and fluid
- constriction of renal arterioles -> DEC GFR
- increase tubular reabsorption
- stim of renin release -> INC angiotensin II and aldosterone -> INC tubular reabsorption
T/F: Angiotensin II level generally have a big impact on extracellular fluid or blood volume
FALSE; little impact
-Angiotensin II is a powerful controller of SODIUM EXCRETION
T/F: a small increase in blood pressure causes an increase in sodium excretion when sodium levels rise
TRUE - due to angiotensin II
Salt sensitivity
a little bit of salt will cause a large increase in blood pressure
-in these patients, renin secretion can NOT be decreased; NEED higher BP to excrete excess sodium
Increased Aldosterone will cause
- INC sodium and water REABSORPTION in the cortical collecting tubules
- INC potassium excretion
Increased ADH will cause
- INC reabsorption of fluid
- concentrated urine
Decreased ADH will cause
- REDUCED reabsorption of fluid
- decreases fluid volume in the body
Omsoreceptor-ADH Feedback System
- water defecit
- osmoreceptor cells in the Anterior Hypothalamus SHRINK
- osmoreceptors cells fire and stimulate the Posterior Pituitary to RELEASE ADH
- ADH transported in blood to kidneys
- LATE DISTAL TUBULE, CORTICAL COLLECTING TUBULES, and MEDULLARY COLLECTING DUCTS increase water permeability
- water reabsorption, and excretion of concentrated urine
AV3V region
- anteroventral region of the third ventricle
- signals posterior pituitary to release ADH
Arterial baroreceptor reflexes
decreased arterial pressure causes an increase in ADH
Cardiopulmonary reflexes
Decreased blood volume causes an increase in ADH
Other things that increase ADH secretion
- nausea
- hypoxia
- drugs (morphine, nicotine, cyclophosphophamide)
Inhibitors of ADH
- alcohol
- clonidine
- haloperidol
Mechanisms that increase sodium excretion
1) activation of low pressure receptor reflexes in the right atrium and pulmonary vessels
2) suppression of Angiotensin II
3) Stimulation of natiruretic system
4) Small increase in arterial pressure
What happens to ECF and blood volume when there’s a leakage of fluid into the interstitium?
INCREASE in ECF
blood volume remains same or decreases
- kidneys sense a decrease in blood volume
- respond by retaining salt and fluid
- retained fluid leaks into interstinum (increased edema)
What happens to ECF and blood volume during congestive heart failure? (or anything that increases vascular capacity, i.e. pregnancy, vericose veins)
INCREASE ECF (200%) INCREASE blood volume (15-20%)
- heart reduces ability to pump = decreased output
- kidneys retain salt and fluid to normalize pressure
- work well; however, extra fluid
What happens to ECF and blood volume during Nephrotic Symdrome?
INCREASE ECF
blood volume remains the SAME
- loss of large amounts of PROTEIN in urine
- osmotic pressure in capillaries falls
- fluid moves from capillaries to tissues
- causes BP to fall
- kidneys activate measures to retain water/sodium
What happens to ECF and blood volume during Liver Cirrhosis?
INCREASE ECF
blood volume remains the SAME
- liver cannot synthesize enough plasma proteins
- osmotic pressure in capillaries falls
- fluid moves from capillaries to tissues
- causes BP to fall
- kindeys activate measures to retain water/sodium
- liver develops fibrous tissue = impedes portal blood flow
- raises capillary pressure in the portal vascular bed
- leakage of fluid and proteins into the peritoneal cavity
