Control of Sodium and Water eXcretion Flashcards
Discuss the 3 types of regulation of BP– which ones does the kidney contribute to
Short-Term BP Regulation: This occurs over seconds to minutes and involves theclassic baroreceptor reflex. It rapidly modulates BP during activity and postural changes. A major regulated parameter is the resistance of thevascular tree.— THIS IS MORE CV AND HAS CAORITD AND AORTIC ARCH SENSORS and in the ATRIA AND PULMONARY VACULATURE.
Medium-Term BP Regulation: This occurs over minutes to hours and involves renal BPsensors that trigger production of a chemical agent (renin) to correct or adjust BP. Again,
a major regulated parameter here is the resistance of the vascular tree.
Long-Term BP Regulation: This occurs over hours to days and involves renal regulation of salt and H20 to actually change the fluid volume in the vascular tree.
Explain Medium term regulation
Renal sensing invovles the granular cells at the JGA. They are not nerve cells that signal the brain stem, but they recieve sympathetic input from the brain. When renal afferent arteriolar pressure is low (or in response to sympathetic input), the granular cells release
the peptide hormone renin.
AA Pressure low— Secrete Peptide hormone Renin— Renin cleaves Angio to make Angio I— ACE then convers Angio I to Angio II which is a vasoconstrictor.
Release of renin triggered by So renin triggered by low BP causes vasoconstriction of AA, decreases filtration and increases BP,
- Renin is secreted when there is a decrease in renal AA pressure and this is sensed by the macula densa sensing of NaCl and the rate of Na+ reabsorpton.
- Also increase in Sympathetic activity caused by decrease in BV wil trigger Renin release
Explain what happens in hemorage
INcrease Fluid reabosrption at Proximal and decrease afferent arteriolar pressure so both cause less NaCl to Macula Densa and increase Renin secretion
What regulate BP long term? Explain it
Blood volume!! Short and medium help compensate for acute blood volume changes but the kdineys handle long term reuglation.
What is natriuresis? Explain it
Exretion of excess Na in urine and whne due to increase pressure it is called pressure natruresis.
- Largely Hemodynamc- drive more Na+ into the nephron then more comes out in urine– this works to decrease BP correcting for the increase that elevated GFR initially
- DOes not involved sensors or circulating facrots
- Is largely a proximal nephron phenomenon
Overall pressure naturesis can help control blood volume but not helpful in controlling water and Na+ independently
Aldosterone Regulation of Na+ Balance
This is the most important control of Na+ reasbsoption indepdnetn of H20
Aldo facts
- Produced in the adrenal cortex
- Controlled by the circulating levels of angio II– angio stimulates the release of aldosterone
- Acts on the CD increasing Na+ reabsorption increasing BV so long term increase in BP
How much Na+ is subject to Aldosterone? Why?
Indeed, only 2% of filtered Na+ is actually subject to aldosterone
regulation. A person will excrete ~2% of filtered Na+ in the complete absence of aldosterone and excrete virtually no Na+ when a maximal plasma aldosterone concentration is present. 2% (522mmoles/day= 30 grams of table salt) is huge when
Total Na+ filtered per day = GFR (per day) x PNa
= 180 L/day x 145 mmoles/L
= 26,100 mmoles/day
RDA of of Na
2.4 g (1 teaspoon)
What type of hormone is aldosterone? How does it work?
Steroid! So if diffuses!
can freely cross cell membranes and thus
simply diffuses into its target cell (i.e. the principle cell). In the cell, it combines with mineralocorticoid receptors in the cytoplasm and then the bound-receptor moves to the nucleus
where it promotes gene expression and synthesis of new mRNA. The result is production of newproteins that increase the activity (or number) of, 1) apical Na+ channels and 2) basolateral Na-
K-ATPase pumps. This promotes increased Na+ reabsorption.
Two signals that stimulate aldosterone release
1. K+ explain later
2. INcrease in angio II- renin secretion (macula densa, renal sympathetic) increase angio II increases aldosterone
What works with (or against) aldosterone to control Na+ balance?
ANP- atrial natriuretic peptide and it promotes Na_ excretion and is sensed in the heart by the atria and the stimulus is distension of the atria (high volume due to high salt)
3 fold function
1. in kidney realxes the AA increasing GFR
- Inhibits reabsoprtion of Na+ in CD
- Inhibits renin-angio-aldosterone system by stopping renin release and stopping angio stimulation of aldosterone.
ADH two functions
1- the main action of ADH is to increase H2O permeability of the collecting duct (thus decreasing H2O excretion).
- ADH also increases Na+ reabsorption by the cortical collecting duct (as does aldosterone). This secondary ADH action seems to synergize with the action of aldosterone and cause even more robust Na+ reabsorption (than with aldosterone alone).
What other hormones can effect Na+ reabsorption? WHne
Estrogen, growth hormone, estrogen, thyroid hormone
Thismay occur when there are abnormally high levels of these hormones.
What is osmolarity of fluid entering the CD
It’s hypoosmotic so there is there is substantial driving force of water out of the CD. But without ADH there is low permeability and that water is excreted.
What woudl increase ADH secretion
- Decrease in BV- like due to hemorrage or diarhea- sensed by the barorecepotrs- when they fire less they stimulate the release of ADH— at very high concentration ADH can cause vasoconstrictorion increasing peripheral resistance and increasing BP
- Osmoreceptors0 increased osmolority sensed by the osmoreceptors in the hypothalamus that communicate to the neurons to release ADH
ADH secreting cells integrate both to decide what to do but osmolarity is important factor
