Homeostatic Regulation of Na Flashcards
2 things that can happen to the extracellular compartment if the number of sodium ions in the body increases
Extracellular compartment can increase in osmolarity
Extracellular compartment will increase in size as water is added to preserve the osmolarity
Effective circulating volume
Basically the blood volume
It is a fixed fraction of the total extracellular volume
This statement changes in disease states
Where are low pressure sensors in the body?
Atria, ventricles (R) and pulmonary circulation
Where are high pressure sensors in the body?
Carotid artery
Aortic arch
Renal arteries
Low pressure sensors
location, stimulation, response
Located in areas of lower BP (atria, RV, pulmonary circulation) where changes in blood volume do not cause large changes in blood pressure
Stimulus: increasing pressure/stretch
Response: inhibition of ADH, release of ANP and BNP
Low pressure sensors sense _____
High pressure sensors sense ____
Low: stretch/increasing pressure (volume)
High: decrease in arterial pressure (pressure)
Net effect of low pressure sensor activation
Increases blood volume here suggests increased ECFV so it is sensed as an increase in total body salt and water
Decrease in ADH allows more water excretion
ANP and BNP allow more natriuresis
Shrink blood volume
High levels of BNP suggest what disease?
Congestive heart failure
High pressure sensors
location, stimulation, response
Stretch receptors in the carotid artery, aortic arch and arterioles of the kidney, that are more sensitive to pressure than volume
Stimulus: decrease in arterial pressure
Response: increase in sympathetic NS activity, increase ADH release, activate RAAS, inhibit ANP
What physiologic effects does increased sympathetic NS activity (from decreased circulating volume) have?
Increase HR, CO Increase vascular tone Decrease GFR Increase renin secretion Increase renal Na reabsorption Overally: decrease renal Na excretion to raise the effective circulating volume
Sodium handling: filtration across the glomerular basement membrane
NaCl is in solution and is freely filtered across the BM
[Na] at the start of the proximal tubule = serum [Na]
Sodium handling: proximal tubule
The cells themselves are almost completely free of Na because of the basal Na/K ATPase
60% of filtered Na is reabsorbed here
Mostly via the Na/H antiporter, Na/glucose co-transporter, or Na/AA co-transporter
This is not a site for potent diuretics (a lot of time to reabsorb later)
Further down a Cl gradient is established and NaCl can be passively reabsorbed
At the end the [Na] is the same as plasam
Sodium handling: loop of henle
Important site for reabsorption of ~25% of filtered Na, but less water
Powered by basolateral Na/K ATPase
Na/K/2 Cl symporter brings ions in with concentration gradient (but needs ATP)
Loop diuretics inhibit what channel
NKCC2
Used when ECF volume overload is suspected
Sodium handling: distal tubule
Early part reabsorbed NaCl without water
Na/Cl symporter is the main channel
Thiazide diuretics inhibit what channel
The Na/Cl symporter (NCC)
Not as potent as loop diuretics but are commonly used to treat hypertension
2 main sites that Na can be excreted from
Loop of Henle
DCT
Sodium handling: collecting duct/tubule
Principal cells carry out NaCl reabsorption via an ENaC
Site of action of aldosterone (increase Na reabsorption in exchange for K excretion)
Aldosterone antagonists
K sparing diuretics
Inhibit the cells in the collecting duct that exchange Na for K
Main prostaglandin in the kidney
PGI2
Effect of prostaglandins on the kidney
Afferent arteriolar vasodilation and natriuresis
In response to Na conserving and vasoconstricting stimuli
In healthy subjects, there is little or no basal PGI2 synthesis
Renal effects of ANPs
Increased GFR
Natriuresis (K sparing)
Antagonism of almost all actions of the RAAS
Uroguanylin
Gut natriuretic peptide
Produced in the intestine in response to salt intake
Reduced renal Na reabsorption, helping to compensate for the ingestion of dietary Na
Not yet a target for intervention
Increased ANP and BNP from an increased effective circulating volume causes…
Increased GFR Decreased renin secretion Decreased aldosterone secretion Decreased Na reabsorption Overall: Increased Na and H2O excretion
