W05: Physiology Cont. - VOLUME REGULATION

Question 1

Describe the components of the renin-angiotensin-aldosterone system

Answer 1

renin produced in JG cells and act on angiotensinogen
*renin release is rate limiting step

ACE found in vascular endothelium

Ang.II stimulates aldosterone secretion (zona glomerulosa adrenal) = Na+ reabs

• RENIN CONVERTS ANGIOTENSINOGEN TO ANG. I in plasma
• ACE converts AngI to Ang.II in plasma

Question 2

List the effects of angiotensin II.

Answer 2

Angiotensin II acts on blood vessels to stimulate vasoconstriction (increases blood pressure). It also acts on the adrenal gland to stimulate the release of aldosterone, which acts on the kidneys to stimulate reabsorption of salt and water, causing fluid volume and blood pressure to increase

Question 3

Most potent osmoles for ECF and ICF

Answer 3

ECF = Na+ and Cl-; where Na+ regulation dependent on high and low p baroreceptors

ICF = K+

Question 4

Describe the renal responses to hypovolaemia.

Answer 4

⇩ECF

⇧salt&H2O loss = ⇩PlVol. = ⇩venous P = ⇩VenousRet. = ⇩atrial P = EDVol = ⇩SV = CO = ⇩BP

detected by sinus baroreceptor thus ⇩inhibition

= ⇧SYMP. DISCHARGE = ⇧VASOCONSTRICTION ⇧TPR = ⇧BP

+ADH++ = hypo-osmol. urine; water retention

+symp. vasoconstriction = renal arterial VC + ⇧renin release = Ang.II
= ⇧NaCl and H2O reabs @ prox tubule
= ⇧Aldosterone = ⇧distal tubule NaCl + H2O reabs.

Question 5

Effect of sympathetic vasoconstriction

Answer 5

renal VC results in ⇧RENIN

= ⇧ANG.II = ⇩peritubular cap hydrostatic P = thereby ⇧Na reabs from tubule = ⇩Na excreted

as well as AngII ⇧aldosterone = ⇧distal tubule Na reabs

Question 6

Hypovolaemic and Hypervolaemic effects on pressure in peritubular caps

Answer 6

HYPO
P(pc) < normal d/t constriction + πp > normal d/t lost NaCl and H2O so ⇧[plasma protein]
= reabs of filtrate up to 75%

HYPER
P(pc) > normal d/t dilation + πp

Question 7

Significance of JG

Answer 7

Juxtaglomerular apparatus formed by JG AND MACULA DENSA important to the aldosterone reflex

JG produce RENIN
• ⇧renin when ⇩afferent P @ JG
• ⇧symp nerve activity = ⇧renin via B1
• Renin inversely proportional to NaCl delivery at macula densa
• Ang. II neg feedback of renin
• ADH inhibits renin release

*RENIN CONVERTS ANGIOTENSINOGEN TO ANG. I in plasma

Question 8

Significance of Ang.II

Answer 8

in hypovol important:

• stimulates aldosterone = h2O retention
• potent vasoconstrictor = ⇧TPR
• stimulates ADH secretion (hypoth) = ⇧H2O reabs from CD
• stimulates thirst and salt appetite (hypoth)

Question 9

Responses to ⇧GFR

Answer 9

Macula densa senses ⇧flow from ascending thick loop segment
= paracrine vasoconstriction of afferent arterioles
= ⇧resistance in afferent = ⇧hydrostatic P in glomerulus = ⇩GFR

Question 10

Patient with severe diarrhoea attempts to replace 3l fluids lost by consuming 2l of fluid

Answer 10

⇩ECF osmolarity as dilution d/t pure water replacement
= ADH (-) via osmoreceptors

BUT
ECF vol lost = ADH(+) via baroreceptors

= VOLUME CONSIDERATION primarily takes importance (baroreceptors) thus ADH (++) although association with hypoosmolarity.

=ensures brain perfusion

Question 11

Significance of ANP

Answer 11

Na+ EXCRETION = H2O release; counters aldosterone in ECF REGULATION
(secreted from atrial cells stimulated by ECF volume expansion)

Question 12

Significance of Aldosterone, and relationship to ANP

Answer 12

Healthy

• Na+ retention and K+ loss = H2O retention
• Followed by spontaneous diuresis 2º to volume expansion (reactive ANP action)
• K+ loss persists due to continued K+ loss

Question 13

Why are Conn’s syndrome patients not hypernatraemic

Answer 13

conn’s syndrome is 1º hyperaldosteronism = promote Na+ retention

BUT it is countered by the action of ANP thus Na+ loss facilitated but K+ (d/t aldosterone) continues and become depleted.

> renin inhibition (renin => aldosterone) in order to stop pathway and oppose Ang.II = Na+ excretion

Question 14

Explain the way in which hyperglycaemia in diabetes mellitus causes osmotic diuresis

Answer 14

Hyperglycaemia will result in exceeding Tm(glc) thus Glc will be lost in urine. As it remains in the tubule, Glc becomes concentrated and in fact draws water from ISF to tubule = diuresis.

+thus [Na+] decreased (tubule) d/t greater dilution effect. = ⇩Na reabs = ⇩⇩Glc reabs d/t ⇩potency of SYMPORTER

+descending loop: H2O retention thus fluid is hyperosmotic thus ASCENDING LOOP fluid is less concentrated = reduced horizontal gradients
= large diuresis + natriuresis

+Na reabs @ distal tubule decreased d/t large delivery of NaCl + H2O inhibits renin release

= excretion of 8L of isotonic urine/day = ⇩plasma vol. = ADH stimulated but useless d/t interstitial gradient abolished

=HYPERGLYCAEMIC COMA (severe hypotension to brain)