Editing Homeostasis (section)

===Sodium concentration===
{{Main |Renin–angiotensin system}} {{Further |Sodium in biology |Tubuloglomerular feedback |Sodium-calcium exchanger}}
The homeostatic mechanism which controls the plasma sodium concentration is rather more complex than most of the other homeostatic mechanisms described on this page.

The sensor is situated in the [[juxtaglomerular apparatus]] of kidneys, which senses the plasma sodium concentration in a surprisingly indirect manner. Instead of measuring it directly in the blood flowing past the [[juxtaglomerular cell]]s, these cells respond to the sodium concentration in the [[nephron|renal tubular fluid]] after it has already undergone a certain amount of modification in the [[proximal convoluted tubule]] and [[loop of Henle]].<ref name=tortora3>{{cite book |last1= Tortora |first1= Gerard J. |last2=Anagnostakos|first2=Nicholas P.| title=Principles of anatomy and physiology |url= https://archive.org/details/principlesofan1987tort |url-access= registration |pages=[https://archive.org/details/principlesofan1987tort/page/420 420–421]|edition=  Fifth |location= New York |publisher= Harper & Row, Publishers|date= 1987 |isbn= 978-0-06-350729-6 }}</ref> These cells also respond to rate of blood flow through the juxtaglomerular apparatus, which, under normal circumstances, is directly proportional to the [[arterial blood pressure]], making this tissue an ancillary arterial blood pressure sensor.

In response to a lowering of the plasma sodium concentration, or to a fall in the arterial blood pressure, the juxtaglomerular cells release [[renin]] into the blood.<ref name=tortora3 /><ref>{{cite journal|title=JAMA Article Jan 2012|journal=JAMA|volume=280|issue=13|pages=1168–72|doi=10.1001/jama.280.13.1168|pmid=9777817|year=1998|last1=Preston|first1=Richard A.|last2=Materson|first2=B. J.|last3=Reda|first3=D. J.|last4=Williams|first4=D. W.|last5=Hamburger|first5=R. J.|last6=Cushman|first6=W. C.|last7=Anderson|first7=R. J.|doi-access=free}}</ref><ref name="isbn0-07-146633-9">{{cite book |veditors=Loscalzo J, Fauci AS, Braunwald E, Kasper DL, Hauser SL, Longo DL | title = Harrison's principles of internal medicine | publisher = McGraw-Hill Medical | location =New York | year = 2008 | isbn = 978-0-07-146633-2 |vauthors=Williams GH, Dluhy RG | chapter = Chapter 336: Disorders of the Adrenal Cortex }}</ref> Renin is an enzyme which cleaves a [[Peptide#Notes on terminology|decapeptide]] (a short protein chain, 10 amino acids long) from a plasma [[Alpha globulin|α-2-globulin]] called [[angiotensinogen]]. This decapeptide is known as [[Angiotensin#Angiotensin I|angiotensin I]].<ref name=tortora3 />  It has no known biological activity. However, when the blood circulates through the lungs a pulmonary capillary [[Endothelium|endothelial]] enzyme called [[angiotensin-converting enzyme]] (ACE) cleaves a further two amino acids from angiotensin I to form an octapeptide known as [[Angiotensin#Angiotensin II|angiotensin II]].  Angiotensin II is a hormone which acts on the [[adrenal cortex]], causing the release into the blood of the [[steroid hormone]], [[aldosterone]]. Angiotensin II also acts on the smooth muscle in the walls of the arterioles causing these small diameter vessels to constrict, thereby restricting the outflow of blood from the arterial tree, causing the arterial blood pressure to rise. This, therefore, reinforces the measures described above (under the heading of "Arterial blood pressure"), which defend the arterial blood pressure against changes, especially [[hypotension]].

The angiotensin II-stimulated [[aldosterone]] released from the [[zona glomerulosa]] of the [[adrenal glands]] has an effect on particularly the epithelial cells of the [[distal convoluted tubules]] and [[collecting ducts]] of the kidneys. Here it causes the reabsorption of sodium ions from the [[Nephron|renal tubular fluid]], in exchange for potassium ions which are secreted from the blood plasma into the tubular fluid to exit the body via the urine.<ref name=tortora3 /><ref>{{cite journal |vauthors=Bauer JH, Gauntner WC |title=Effect of potassium chloride on plasma renin activity and plasma aldosterone during sodium restriction in normal man |journal=Kidney Int. |volume=15 |issue=3 |pages=286–93 |date=March 1979 |pmid=513492 |doi= 10.1038/ki.1979.37|doi-access=free }}</ref> The reabsorption of sodium ions from the renal tubular fluid halts further sodium ion losses from the body, and therefore preventing the worsening of [[hyponatremia]]. The hyponatremia can only be ''corrected'' by the consumption of salt in the diet. However, it is not certain whether a "salt hunger" can be initiated by hyponatremia, or by what mechanism this might come about.

When the plasma sodium ion concentration is higher than normal ([[hypernatremia]]), the release of renin from the juxtaglomerular apparatus is halted, ceasing the production of angiotensin II, and its consequent aldosterone-release into the blood. The kidneys respond by excreting sodium ions into the urine, thereby normalizing the plasma sodium ion concentration. The low angiotensin II levels in the blood lower the arterial blood pressure as an inevitable concomitant response.

The reabsorption of sodium ions from the tubular fluid as a result of high aldosterone levels in the blood does not, of itself, cause renal tubular water to be returned to the blood from the [[distal convoluted tubule]]s or [[collecting duct]]s. This is because sodium is reabsorbed in exchange for potassium and therefore causes only a modest change in the [[Osmotic pressure|osmotic gradient]] between the blood and the tubular fluid. Furthermore, the epithelium of the distal convoluted tubules and collecting ducts is impermeable to water in the absence of [[Vasopressin|antidiuretic hormone]] (ADH) in the blood. ADH is part of the control of [[fluid balance]]. Its levels in the blood vary with the [[osmolality]] of the plasma, which is measured in the [[hypothalamus]] of the brain. Aldosterone's action on the kidney tubules prevents sodium loss to the [[extracellular fluid]] (ECF). So there is no change in the osmolality of the ECF, and therefore no change in the ADH concentration of the plasma. However, low aldosterone levels cause a loss of sodium ions from the ECF, which could potentially cause a change in extracellular osmolality and therefore of ADH levels in the blood.