Lecture 3: Regulation of osmolarity by regulation of H2O reabsorption (ADH), regulation of volume by regulation of Na+ reabsorption (RAA, ANP, and BNP)

what’s the other name for ADH

vasopressin

AQP2 is regulated by

ADH

water reabsorption is

solute-free. it dilutes the plasma, decreasing Posm toward normal

when water is added to ECF, why does plasma volume not change significantly?

constant shift between ECF and ICF (which holds 2/3 of total body water)

what are the regulators of ADH release

• increased osmolarity (most important)

• decreased arterial pressure (arterial baroreceptor input)

• decreased arterial stretch due to low blood volume

effect of alcohol on ADH release

inhibits ADH release (increased urination b/c water isn’t being reabsorbed)

effect on arterioles is only at

high levels of ADH

effect on kidneys is at

all levels of ADH

ADH controls kidney/CD h2o reabsorption via

high affinity V2 receptor, meaning strong effect at low levels of ADH

ADH acts as a vasoconstrictor on vascular smooth muscle via

low affinity V1 receptor

ADH secretion is most sensitive to which change (plasma osmolarity, volume, pressure)?

osmolarity

explain what happens with high plasma Osm and urine concentration

1. high plasma Osm

2. high ADH

3. high water reabsorption in CD

4. high solute free water reabsorption

5. dilutes plasma osm toward normal

6. excretion of highly concentrated urine

explain what happens with low plasma Osm and urine concentration

1. low plasma Osm

2. low ADH

3. low water reabsorption in CD

4. high solute-free water excretion

5. concentrates plasma Osm toward normal

6. excretion of a highly dilute urine occurs

where is ADH secreted

hypothalamic neurons in the posterior pituitary

what is the primary sensory input for ADH secretion

osmoreceptors in the hypothalamus

where are arterial baroreceptors located

aortic arch and carotid arteries

how is thirst mechanism regulated

• decreased plasma volume → decreased MAP → arterial baroreceptors → increased renin → increased angiotension II → thirst

• increased plasma osmolarity → osmoreceptors → thirst

Na+ excretion equation

regulation of ECF volume occurs via

changes in Na+ excretion which cause changes in H2O excretion (because H2O follows Na+)

what is the relationship between Na and ECF volume

increased NaCl load → increased volume as measured by body weight (initial response)

regulation of Na+ excretion occurs in response to changes in

blood pressure via an arterial baroreceptor-mediated response

how is Na+ reabsorption regulated on proximal tubule

increased by angiotensin II

how is Na+ reabsorption regulated on distal tubule

increased by angiotensin II

how is Na+ reabsorption regulated on collecting duct

increased by aldosterone

explain mechanism of renin secretion via extrarenal control

increased sympathetic activity → increased renin secretion by juxtaglomerular cells

explain mechanism of renin secretion via intrarenal control

decrease pressure in afferent arteriole → intrarenal baroreceptors on juxtaglomerular cells respond → increased renin secretion

explain mechanism of renin secretion via NaCl delivery

constriction of afferent arterioles → low GFR → low NaCl delivery to macula densa cells → altered paracrine factors (e.g., decreased ATP and adenosine, increased prostaglandins) → increased renin release

renin-angiotensin-aldosterone (RAA) system

action of aldosterone on late distal tubule/cortical collecting duct cell

1. aldosterone combines with a cytoplasmic receptor

2. initiates transcription in nucleus

3. increased ROMK (Renal Outer Medullary K+) channel and increased ENaC (epithelial sodium channels) on apical membrane

4. increased Na/K pump on basolateral membrane

5. result is increased Na+ reabsorption and K+ secretion

renin

hormone (enzyme) released from kidney and is the rate limiting step in the conversion of angiotensinogen to angiotensin II in the plasma

angiotensin II

peptide generated in the plasma and tissue compartments; stimulates aldosterone secretion, Na reabsorption (proximal tubule via NHE3, Na+/H+ exchanger), thirst, ADH secretion, and vascoconstriction

aldosterone

steroid hormone released from adrenal gland; stimulates Na+ reabsorption in the cortical CD of kidneys (by activating ENaC and Na+/K+ ATPases)

does blood volume have to drop for pressure to drop?

No. Heart attack or failure → decreased SV and MAP… however blood volume is unchanged

ECF osmolarity is regulated by

primarily controlling water excretion via alterations in ADH secretion

ECF volume is regulated by

altering the reabsorption and excretion of BOTH Na+ and H2O via RAA and ADH changes

what increases ANP secretion

increased atrial distension

what increases BNP secretion

increased ventricular distension

what happens after increased ANP and BNP

increased GFR → decreased renin → decreased Ang II → decreased aldo and ADH → reduced Na+ and H2O reabsorption → increased sodium and water excretion → volume decreases toward normal

ANP change is NOT due to ________, it is due to __________

increased MAP, it is due to increased VR and EDV, which are often caused by increased volume