water and sodium regulation Flashcards
how is sodium reabsorbed
Sodium reabsorption is an active process occurring in all tubular
segments except the descending limb of the Loop of Henle and the
medullary collecting duct
how is water reabsorbed
Water reabsorption is by diffusion (i.e., osmosis) and is dependent upon
sodium reabsorption (but not exclusively).
Water moves through aquaporin channels. The presence of these aquaporins varies throughout the tubule segments. They are highly expressed in the proximal nephron. They are absent in the collecting ducts unless Anti-diuretic hormone (ADH) is active.
key points of sodium reabsorption
- Active transport out of cells into interstitial fluid.
- Transport achieved by Na+/K+-ATPase pump
- Keeps intracellular conc. of Na+ low to allow
‘downhill’ movement of Na+ from lumen - Mechanism of Na+ movement across luminal
membrane varies between tubule segments,
whereas always via Na+/K+-ATPase pump for
basolateral membrane - Proximal tubule (a): co-transport / counter-
transport of organic molecules (glucose, aa) - Cortical collecting ducts (b): via Na+ channels
what is the make up of water distributions
2/3 intracellular
1/3 extracellular
what does ADH do
Anti-diuretic hormone (ADH) [aka
vasopressin]) initiates a cascade of
event within the collecting duct cells
that leads to an increased number of
AQP2 channels in luminal membrane,
This allows increased passive diffusion of
water into the cell.
Water exits cell through AQP3 and
AQP4, which are not vasopressin
sensitive
what does ADH combine with
ADH uses cAMP systems to cause the
insertion of aquaporins into the
membranes of the principle cells of the
collecting ducts.
So water flows out of the collecting
ducts to be reabsorbed by the body
what regulates ADH
Regulation of ADH release from posterior
pituitary gland.
Most important of the inputs come
from osmoreceptors (primarily) and
baroreceptors
slide 10
slide 10
the 3 factors effecting sodium reabsorption
1) Aldosterone (most major)
2) Atrial Natriuretic Peptide (ANP)
3) Local effect of blood pressure on the tubules
describe the Aldosterone and the
Renin-Angiotensin System
The release of the enzyme renin converts the
peptide angiotensinogen to angiotensin I.
Angiotensin I then converted to angiotensin II
byangiotensin-converting enzyme (ACE).
Angiotensin II acts on angiotensin receptors located in several target tissues including the adrenal glands, kidneys, brain, and vasculature
Activation of angiotensin receptors in the adrenal glands stimulates aldosterone release from these glands, which increase Na+ and H2O reabsorption
slide 13
how does Atrial Natriuretic Peptide (ANP) impact sodium regulation
ANP is synthesized and sorted in atrial myocytes
ANP is released in response to stretching of the
atria
This occurs when our circulating blood volume increases
An increase in circulating levels of ANP causes ↑Na+ excretion
how does Local effect of blood pressure on the tubules effect sodium regulation
Baroreceptor regulation of blood pressure simultaneously
regulates total-body sodium
» See figure summarising major mechanisms wherein Na+
loss elicits a decrease in GFR.
This is affected by the volume of surface available,
filtration membrane permeability and NFP (net
filtration pressure), blood pressure / blood flow to
the glomerular capillaries.
» GFR is directly proportional to NFP. Therefore,
increases (or decreases) in systemic blood pressure
causes increases (decreases) in GFR
what do diuretics do
Diuretics are substances that promote the loss of Na+ and H2O
diuretics as medications
Diuretics can be medications use to help the body remove excess sodium and waterand
help control blood pressure
» Osmotic diuretics; carbohydrates that are filtered but not reabsorbed (ex. Mannitol).
» Loop diuretics (lasix, furosemide) are the most powerful diuretics because they inhibit the formation of the medullar gradient by inhibiting Na+ reabsorption.
» Hydrochlorithiazide acts on the distal collecting duct.
» Spironolactone is an aldosterone receptor antagonist. This is known as a K+ sparing diuretic. It acts because the K+ in the urine is from aldosterone-driven active tubular secretion into the late DCT and collecting ducts
how do exercise impact renal function
Renal blood flow decreases as soon as exercise starts
Linear relaƟonship: ↑ exercise intensity = ↓renal
blood flow
describe the renal blood flow during exercise
Increase sympathetic nervous system activity during exercise causes vasoconstriction of
the renal arterioles.
↑ exercise intensity = ↑ sympatheƟc nervous system acƟvity = ↓renal blood flow
Increase ADH (or vasopressin) release also reduces renal blood flow
ADH causes renal vasoconstriction
Remember that ADH release activity due to renin-angiotensin-aldosterone system
Despite renal blood flow, increase work for the kidney during exercise
how do the kidneys maintain PH during exercise
via loss of excess H+ in the urine
Kidneys removes a small amount (2%) of total lactate produced
during exercise
how does the kidney conserve body water during exercise
fluid regulatory hormones act to increase
water and Na+ reabsorption in the kidney
how does the kidney excrete metabolites during exercise
H+
Creatinine (excess created from muscle breakdown)
Other proteins
what is rhabdomyolysis
A condition where skeletal muscle cell
damage can cause acute renal failure
and sometimes death
what increases the chances of rhandomyolysis
Rhabdomyolysis is most often observed with novel, strenuous,
overexertion
» heat stress ↑ risk
» dehydration likely ↑ risk
