Ch 20 - Fluid and electrolyte balance

integrated responses to change blood volume/pressure

response to decreased - increase CO, increase thirst to increase water intake, kidneys conserve salt and water to minimize volume loss

response to increase - lower CO, excrete salts and H2O in urine

osmotic gradient in renal medulla

# of solutes in 1 kg of water, reflects ability to cause osmosis, kidneys maintain osmolality of plasma (in cortex) at 300 mOsm, deeper into renal medulla is more concentrated; concentration changes throughout nephron (descending limb only water leaves so concentration gets higher, ascending opposite)

countercurrent mechanism

occurs when fluid flows in opposite directions on two adjacent segments of same tube with hair pin tube (think its flowing down in descending tube then up in ascending)

key players of countercurrent mechanism

countercurrent multipliers - long nephron loops create the gradient

countercurrent exchangers - blood vessels nearby preserve the gradient

collecting ducts - use the gradient to adjust urine osmolality

juxtamedullary nephron is critical

countercurrent multipliers

long nephron loops create the osmotic gradient, three properties - fluid flows in opposite direction in to adjacent sections, descending limb is permeable to water not salt (filtrate osmolality increases), ascending limb is permeable to salt not water (osmolality decreases to dilute filtrate more than initial); creates positive feedback b/c salt leaving makes more water want to leave descending limb next time from fluid osmolality (not filtrate); constant 200 mOsm difference between 2 limbs of nephron loop/between ascending limb and interstitial fluid

countercurrent exchangers

vasa recta preserves gradient, vasa recta is highly permeable to water and solutes, blood is isosmotic to the surrounding fluid, it doesn't undo gradient, concentrations mirror nephron loop

collecting duct

use medullary gradient, under control of ADH/vasopressin (increases water in blood), high ADH=collecting duct highly permeable and water leaves=concentrated urine; low ADH=collecting duct impermeable to water=low concentrated urine

how does ADH/vasopressin affect permeability

vasopressin from blood stream travels to membrane receptor on collecting duct cell - activates cAMP system - cell inserts aquaporin channels opening from cell to collecting duct lumen = water is absorbed by osmosis across the cell to the bloodstream

production and release of vasopressin

made and packaged in vesicle in cell body of neuron, vesicle is transported to posterior pituitary, when stimulated its released into blood; stimulation can be decreased bp, decreased atrial stretch, osmolality higher thaan 280 mOsm

homeostatic responses to salt ingestion

ingest salt - no change in volume but increase osmolality - increase vasopressing so kidneys conserve/reabsorb more water or increase thirst to increase water intake - goal to return osmolality to normal as well as bp and volume

aldosterone/RAS

maintains Na balance in body, water wants to follow; decreased bp either causes increase in symp activity or decreases Na present which is detected by macula densa - granular cells of afferent arteriole produce renin - converts angiotensinogen in plasma to ANG 1 - ACE enzyme converts ANG 1 to ANG 2 - ANG 2 has many effects to increase bp/bv/maintain osmolality (vasoconstriction, increase CO, increase vasopressin, increase aldosterone and Na reabsoprtion)

atrial natriuretic peptides

increased blood volume causes atrial stretch, too much is too bad, natriuretic peptides released - work to decrease bv/bp (less vasopressin, less Na reabsorption, increase GFR, less aldosterone, less renin, less symp output)