Plasma Volume & Osmolarity Flashcards
Volume & Composition
Largest fraction of body fluid inside cells= ICF
ICF has high K+/low Na+ fluid
ECF is high Na+/low K+
Cells maintain ICF to ensure metabolic activity & control movement of solutes & fluid. If ECF composition changes- cells lose control.
ECF divided into IF & plasma. SEparated by non selective endoth layer of caps so ECF & IF composition identifical!
Kidney turns ove 12x per 24 hr.
ECF= 3 L + 11 L
ICF= 28 L
for 70 kg man ~42 L of fluid
H2O balance
Take in 2.5 L of H2O/day from metabolism 500 mL. food 500 mL & drinking 1.5 L.
Kidney, GI, resp. skin losses balance consumption
Kidney reg intake/excretion of insensible losses through other systems.
ECF Osmolarity Control
Change in H2O content causes change in osmotic P of ECF due to NaCl changes
H2O excreted in kidneyes (hormones)
Thirst mech
ADH release modulated by vol
Normal control of ADH release is by changes in osmotic P of plasma. Mech high sensitive: above 280 mOSm/kg H2O= linear relationship b/t plasma osmolarity * plasma ADH []
ADh release altered by change in blood vol. If blood vol decreased by more than 10% then increased ADH release
Effect of PV modulates release of ADH so that at increased BVol response blunted & decreased BVol response potentiated!
ADH [] & Urine osmolarity
Release of ADH & plasma osmolarity tightly coupled- plasma osmolarity increases result is plasma [ADH] brings almost perfect compensatory change in urine osmolarity.
ADH Release
ADH release from post pit is controlled by hypothal!
Inputs from both high P baroR & low P vol R
Changes in afferent input form these R, alter rate of ADH relase
Vol Sensors
BaroR:
Vascular sys:
- Low P= cardiac atria (secrete ANP) & pulm vasculature
- High P= carotid sinus, aortic arch, afferent arteriole (renin secretion)
ADH Control
Feedback Mech
Control of Thirst
Very sensitive, plasma [Na+] increase of 2 mmol/L sufficient!
Response to Change in Na+ Intake
NaCl major electrolyte- total amt of NaCl in body determines vol of ECF.
Kidney lags in its response to increase Na+ excretion. During period + Na+ balanceds! Extra Na+ & Cl- exert osmotic P so fluid retained in ECF- vol of ECF increased & so does BW & BP!
No change in [Na+] & ICFV!
When dietary intake returned to normal, kidneys respond by decreasing Na+ excretion, but kidney lags again & at - Na+ balance.
As excess NaCl excreted the retained fluid is also excreted & BW & BP returned to normal.
ECF Vol control
Vol controlled via detection of circulating vol.
Vol R in vascular sys (baroR)
Control of Na+ excretion
- Glomerulotubular balance
- Renin-Angiotensin-aldosterone
- Symp n.
- ADH
- Natriuretic peptides/Factors (Na+ losing)
Effector Pathways
RAAS
Ang II
Ang II increase Na+ reabsorption by altering renal hemodynamics
Ang II constricts efferent more than afferent arteiroles so increase filtration fraction & reduce P hydrostatic in downstream peritubular cpas
Incrased filtration fraction also increases prot [] in pertitubular cpas & raises oncotic P of peritubular caps. Changes in ea of F favor uptake of reabosrbate from peritubular interstitium into peritubular cpas & ehance reabsorption of Na+ 7 fluid by proximal tubule.
Ang II decreases medullary blood flow through vasa recta.
Low blood flow decreases medullary washout of NaCl & urea, process that raises [urea] in med interstitium.
Ang Ii reaises sensitivity & lowers set pt of tubuloglomerular feedback mech
Increase Na+ & fluid delivery to macula densa produce large reduction in GFR
Ang Ii also promotes Na+ reabsorp in PT, thick ascend limb & initial CT by direct effects mostly Na+/exchange- dep pathways!
Symp Nerves
- Afferent & efferent arteriolar [] a; reduced GFR; reduced filtered load
- Increased renin secretion B, increased ang Ii & aldosterone, increased Na+ reabsorption
- Increased Na+ reaborption a by PT
GFR reduced due to vasoconstrictive effects on vessles so reduced filtered load.
Increased renin secretion so raised Ang II & aldosterone levels both increase Na+ reabsorb!
Sym innervate PT epith cells & increase reabsorption
Atrial Natriuretic Peptides
ANP inhibit NaCl & H2O reabsorption
Secretion of ANP by cardiac atria & BNP (brain) by cardiac ventricles stimulated by rise in BP & increase in ECF vol.
ANP & BNP reduce BP by decreasing TPR & enhance urinary excretion of NaCl & H2O
Hormones also inhibit reabsorption of NaCl by medullary portion of CD & inhibit ADH stimulated H2O reabsorption across CD.
ANP & BNP also reduce secretion of ADH from post pit.
These actions mediated by activation of mem bound guanylyl cyclases R which increase cGMP!
Urodilatin
Secreted by distal tubule & CD & not present in systemic.
Secretion stimulated by rise in BP & increase in ECF vol
Inhibits NaCl & H2O reabsorption across medullary portions of CD
Urodilatin more potent natriuretic & diuretic than ANP because some ANP that enters kidneys in blood is degraded by neutral endopeptidase that has no effect on urodilatin
Uroguanylil & guanylin
Produced by neuroendocrine cells in intesinte in response to oral ingestion of NaCl
These hormones inhibit NaCl & H2O reabsorption by kidneys via activation of mem bound guanylyl cyclase R, which increase cGMP
Feedback due to decrease ECFV
Hemorrhage
Summary
Pressure Effect
Pressure diuresis/natriuresis- acute change in BP
Loss of Na+= loss of H2O
= red intravascular vol
= red CO
normalize P!
