Plasma Volume & Osmolarity

Question 1

Volume & Composition

Answer 1

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

Question 2

H2O balance

Answer 2

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.

Question 3

ECF Osmolarity Control

Answer 3

Change in H2O content causes change in osmotic P of ECF due to NaCl changes

H2O excreted in kidneyes (hormones)

Thirst mech

Question 4

ADH release modulated by vol

Answer 4

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!

Question 5

ADH [] & Urine osmolarity

Answer 5

Release of ADH & plasma osmolarity tightly coupled- plasma osmolarity increases result is plasma [ADH] brings almost perfect compensatory change in urine osmolarity.

Question 6

ADH Release

Answer 6

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

Question 7

Vol Sensors

Answer 7

BaroR:

Vascular sys:

• Low P= cardiac atria (secrete ANP) & pulm vasculature
• High P= carotid sinus, aortic arch, afferent arteriole (renin secretion)

Question 8

ADH Control

Answer 8

Question 9

Feedback Mech

Answer 9

Question 10

Control of Thirst

Answer 10

Very sensitive, plasma [Na+] increase of 2 mmol/L sufficient!

Question 11

Response to Change in Na+ Intake

Answer 11

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.

Question 12

ECF Vol control

Answer 12

Vol controlled via detection of circulating vol.

Vol R in vascular sys (baroR)

Question 13

Control of Na+ excretion

Answer 13

1. Glomerulotubular balance
2. Renin-Angiotensin-aldosterone
3. Symp n.
4. ADH
5. Natriuretic peptides/Factors (Na+ losing)

Question 14

Effector Pathways

Answer 14

RAAS

Question 15

Ang II

Answer 15

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!

Question 16

Symp Nerves

Answer 16

1. Afferent & efferent arteriolar [] a; reduced GFR; reduced filtered load
2. Increased renin secretion B, increased ang Ii & aldosterone, increased Na+ reabsorption
3. 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

Question 17

Atrial Natriuretic Peptides

Answer 17

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!

Question 18

Urodilatin

Answer 18

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

Question 19

Uroguanylil & guanylin

Answer 19

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

Question 20

Feedback due to decrease ECFV

Answer 20

Hemorrhage

Question 21

Summary

Answer 21

Question 22

Pressure Effect

Answer 22

Pressure diuresis/natriuresis- acute change in BP

Loss of Na+= loss of H2O

= red intravascular vol

= red CO

normalize P!