• passive (transcellular or paracellular)
• follow osmotic gradient of sodium and other solutes
• function- regulates osmolality of body fluids

• we have osmoreceptors in brain as well as paraventricular and supraoptic nucleus
• this regulates the release of ADH

• water diuresis
• high volume of dilute urine excreted
• CD impermeable to water
• low solute concentration in medullary interstitium

• ADH bind to V2 receptor on principle cell
• act via cAMP second messanger system
• eventually lead to increase insertion of aquaporins

• in condition of antidiuresis
• makes CD very permeable to water
• low amount of concentrated urine excreted

• concentrates solute in medullary intersitium
• high solute concentration enable kidney to excrete highly concentrated urine, conserving water during periods of dehydration
• requires integrated function of:
  • descending/ascending limbs of Henle
  • vasa recta capillaries
  • collecting ducts

• highly permeable to water and solute
• slow blood flow and hairpin turn allows the recirculation of solutes (if you drink a lot of water, fast flow, so you cant recirculate)
• water and salt are exchanged between descending and ascending limbs
• increase flow will reduce medullary osmolarity
• solute gradient maintained while small amounts of NaCl, water returned to blood

• body generate 600 mOsm waste/day
• max urine concentration is 1200 mOsm/L

600/1200 = 0.5 L/day

Clearance osm. = urine osm. x V/plasma osm.

clearance of water = volume - osmolar clearance

*if Uosm < Posm, clearance of water is positive (clear water cleared from body)

*if Uosm > Posm, clearance of water is negative (pure water is retained)

FEx = amount excreted/amount filtered =

(Ux X volume of urine)/(plasma x X GFR)

• increased ECF volume leads to sodium excretion
• decreased ECF volume cause sodium conservation

renal sympathetic nerves

RAAS

aldosterone

ANP/BNP

urodilatin

intrarenal PG's

• renal symp. (directly stimulate)
• TG feedback- decrease NaCl delivery to macula densa, cause renin secretion
• intrarenal baroreceptor- decrease afferent arteriole pressure leads to increase renin secretion

1. decrease body Na contnet
2. decrease effective circulating volume
   1. decrease sodium delivery at macular densa
   2. decrease afferent arteriole pressure
   3. increase symp. activity (baroR)
3. to granular cells
4. increase renin release
5. cleaves angiotensinogen to Ang I

• vasoconstriction (intrarenal, systemic)
• increase PCT reabsorption of sodium
• increase aldosterone release from zona glomerulosa of adrenal cortex
  • increase DCT sodium reabsoprtion
• thirst feelings
• ADH release, leading to water retention

• increase plasma potassium
• increase ACTH
• increase ang II

• principle cells in CD
  • increase Na reabsorption
  • increase K secretion
  • increase H secretion
• intercalated cells in CD
  • increase H secretion

• increase GFR (afferent arteriole dilate, efferent arteriole constrict)
• inhibit sodium reabsoprtion at medullary CD
• suppress renin sec.
• suppress Ald sec.
• systemic vasodilator
• suppress ADH secretion, actions

• secreted by DCT, CD in response to increase arterial pressure and ECF volume
• effects
  • suppress sodium and water reabsorption by medullary CD
  • NO EFFECT on systemic circ. (unlike ANP, BNP)

• increase GFR (dilate renal arterioles)
• supress Na reabsorption in thick ascending limb, cortical collecting duct
• NET EFFECT- increase sodium excretion

• decrease arterial bp
• increas symp. system
  • vasoconstrict
  • increase NaCl PCT reabsorption
• increase renin secretion
• increase Ang II
  • increase NaCl PCT reabsorption
• increase aldosterone
  • increase NaCl CD reabsorption
• NaCl retention increases
• EC volume expansion
• maintain bp

• physiological control exerted at collecting duct
• principal cells secrete potassium
• intercalated cells reabsorb potassium depending on electrochemical gradient at collecting duct

• insulin deficiency
• beta adrenergic antagonist
• alpha adrenergic agonists
• acidosis
• hyperosmolarity
• cell lysis
• exercise

• high insulin
• beta2 adrenergic agonists
• alpha adrenergic antagonists
• alkalosis
• hypoosmolarity

• high potassium diet
• hyperaldosteronism
• alkalosis
• thiazide diuretics
• loop diuretics
• luminal anions

• low potassium diet
• hypoaldosteronism
• acidosis
• potassium sparing diuretics

• high potassium has higher membrane potential (less negative)
• low E.C potassium has much lower membrane potential (more negative- hyperpolarized)

• majority of reabsorption at PCT (67%)
• reabsorption via Na/K/2Cl transporter at thick ascending limb of loop of Henle (20%)

• EC potassium conc.
• sodium concentration in tubular lumen (Na/K exchange)
• luminal fluid flow rate (dilution of secreted potassium)
• E.C pH (K/H exchange) (potassium conc. increase with decreasing hydrogen conc./increase pH)
• Ald (stimulate K secretion at CD)

• reabsorption- H/K pump from lumen into cell while potassium channel cause it to leave into blood
• secretion- Na/K pump from blood into cell while potassium channel cause it to leave into lumen

• cause- aldosterone secreting tumor in adrenal cortex
• effect
  • leads to excessive increase potassium secretion by CD
  • consequence: hypokalemia

• cause- destroy adrenals (NO aldosterone)
• effect
  • decrease potassium secretion in CD
  • consequence: hyperkalemia