Regulation of
Location
fluid homeostasis
Macula densa
cells
Stimulus
Effect/secretion
Secretion effect
Overall effect
Sense osmolality:
increase in Na+
osmolality
 Paracrine from
macula densa
cell
 Sense decrease in
BP such as when
dehydrated or
hemorrhaging
AII
Release paracrine
to JG cells
Paracrine stimulate JC cells to ↑ Renin
secretion
↑ BP back to normal
Renin
Renin converts angiotensinogen 
angiotensin I (AI). ACE in lung convert
AI  AII. AII stimulate aldosterone
secretion & cause systemic
vasoconstriction.
↑ BP back to normal
↑ aldosterone
secretion
Aldosterone affect late distal convoluted
tubules (LDCT) and early collecting –
insert additional ion channels on principle
cells  ↑ Na+ reabsorption, allow K+ to
move from blood to filtrate, if ADH is
present water will follow Na+ into blood
ADH target principle cells LDCT and
early collecting – put on/increase
synthesis of aquaporins (water transporter)
and make cells more permeable to water
↑ BP back to normal
Desire to drink more water and intake
more salt
Hydrate self


↑ BV and BP
JG cells
Afferent
arteriole (AA)
of the
neprhone
Cells in adrenal
cortex
Adrenal cortex
Supraoptic
hypothalamus
Hypothalamus
Sense osmolality:
increase in Na+
osmolality,
dehydration
Neurons in
hypothalamus
Hypothalamus
(thirst center)


Baroreceptors
(extrinsic neural
control)
Aortic arch of
heart & carotid
artery

Increase
production of
ADH
hormone
 Release ADH
from posterior
pituitary
Stimulate thirst
Dry mouth
Osmoreceptors
sense increase in
osmolality
Low BP
Increase in SNS 
↑ nt release in
sympathetic
nerves in the
kidney


Systemic vasoconstriction
Vasoconstriction only at the efferent
arterial (EA)  decrease in fluid loss
at the kidney
Extreme SNS – extreme
vasoconstriction to kidney  ↓ BF to
glomerulus, ↓ GFR and ↓ fluid loss
Stimulate JG cells to release renin
Concentrated urine,
dilute plasma 
decrease osmolality,
↑ blood volume
(BV) and ↑ BP to
normal
Hypovolemic
Hypervolemic
Isovolemic
Hypernatremia
Loss of water and Na+ but losing
more water than Na+ so
concentration of Na+ to water is
relatively high (thus hypernatremia)
Gain of water and Na+ but gaining
more Na+ than water so Na+ conc is
higher relative to water
Loss of water without losing Na+ so
Na+ conc is higher relative to water
ECF volume
Low
Causes
Renal, adrenal, GI, lung,
skin problem
Elevated
Iatrogenic - medically
induced mistake
Normal
Diabetes insipidus , skin
loss, iatrogenic, reset
osmostat
Serum osmolality
Normal
Classification of hyponatremia
Isotonic hyponatremia
Elevated
Hypertonic hyponatremia
Low
Hypotonic hyponatremia
Hypovolemic
Hypervolemic
Isovolemic
Hypotonic Hyponatremia
Very high level of Na+ in
the body
ECF volume
Low
Very high level of Na+ in
the body
Normal body level of Na+
Elevated
Normal w/ sm
increase
Clinical presentation
 Losing water volume to the urine
 ↓BV and ↓BP, ↑ HR
(tachycardia)
 Poor skin turgor
Water accumulating in the IF  edema
Too much urine: diabetes – loss of
water in urine bc lack of ADH
Causes
Hyperlipidemia, hyperproteinemia, isotonic
infusion
Hyperglycemia, hypertonic infusion
Look at ECF volume to determine which type of
hypotonic hyponatremia
Causes
Renal, adrenal
insufficiency, GI, lung,
skin problem
Heart failure, liver
damage, nephrosis
SIADH, renal failure, K+
loss, reset osmostat,
Clinical presentation
Poor skin turgor, tachycardia (↑ Hr),
hypotension (↓BP)
Potassium (level in ECF)
Hyperkalemia – too much K+
Cause
 Too much intake (such
as salt substitutes)
 Renal failure
 Metabolic acidosis
K+ excretion
Low – such as renal
failure where K+ is not
excreted out properly 
too much K+
K+ leaving the cell
High
Hypokalemia – too little K+

High – such as too much
diuretics  losing K+
into the urine
Low


Disturbances
of acid-base
Acidosis
Cause
Contributing cause
Metabolic
Respiratory
Excess H+ ion
or loss of
bicarb

Cause: ↑H or loss of bicarb
Compensation:
 Change respiration: ↑ ventilation
 Kidney: ↑ secretion of bicarb
 Kidney: ↑ excretion of H+ & and
titrate w/ NH3 or PO4 to be
eliminated
Cause: loss H+ or excess bicarb
Compensation:
 Change respiration: ↓ ventilation
 Kidney: ↑ excretion of bicarb
Cause: hypoventilation (↑ CO2 
↑ H+ produce)
Compensation:
 Kidney: retain bicarb to be
reabsorb back to the blood
 Kidney: secrete H+ at PCT
DCT, or intercalated cells
Cause: hyperventilation (↓ CO2 
↓ H+ produce)
Compensation
 Kidney: secrete bicarb

Alkalosis
Too little intake
(unbalance diet)
Diuretics
Metabolic alkalosis
Clinical presentation
 Muscle weakness,
intestinal & cardiac
problem
 Change in ECG
 Cardiac arrest
 Muscle weakness,
intestinal & cardiac
problem
 Respiratory arrest
Excess base
(ingesting too
much) or ↑ H
ion loss

Excess acid production:
diabetic ketoacidosis,
starvation, lactic ketosis,
kidney disease, hyperkalemia
Excessive vomiting – from
the intestine  losing base
 ↓ pH
Mild/moderate vomiting –
lose acid