Wikinotes

Maintainer: admin

most abundant intracellular ion
important for function of excitable tissues
- major determinant of resting membrane potentials
hyperkalemia: high potassium concnetration in extracellular fuid
hypokalemia: low ^
hypo/hyperkalemia both cause abnormal rhythms of the heart
- ex: hyperkalemia and electorcardiogram: as potassium concentration increaes, P wave gets taller, and QRS gets wider, and eventually person goes into cardiac arrest

balance is maintained by kidny because 90% of potassium intake is excreted into urine.
in kidney:
- freely filtered at glomerulus
- but then tubule reabsorb most of the filtered K so very little K actually apppear in the urine
- however, K is secreted at the cortical collecting duct
  - coupled with Na+ reabsorption by K+/Na+ APTase at basolateral membrane and K+ chanel at apical luminal membrane
- change in K excretion is mainly due to K secretion in the cortical collecting duct and some in distal convoluted tubule.

by aldosterone
- hypercolemia --> aldosterone secretion in adrenal cortex --> cortical collecting duct's secretion of potassium increase --> more excretion
  - hypercolemia can also increase secretion of potassium at CCD directly.
K secretion can occur when renin aldosterone system is activated by other causes:
- (remember the pathways that decrease sodium excretion, since aldosterone also inhibits sodium excretion)
- decrease in plasma volume -- >angiotensin --> aldosterone secretion incresases --> sodium reabsorption increase and potassium secretion increase
hyperaldosteronism:
- common cause: adenoma of the adrenal gland that produces aldosterone
- effects: hypertension, hypokalemia,
- renin is suppressed (not sure why)
- metabolic alkalosis (loss of hydrogen ions in urine)

tightly regulated because metabolic reactions are senstivie to pH.
gain of hydrogen ion from CO2 (volatile acid)
- production of nonvolatile acid (phosphoric acid, sulfuric acid, lactic acd) from metaoblism of organic molecules and proteins
- gain of hydrogen due to loss of bicarbonate
  - due to diarrhea (loss of gastric fluid)
  - into urine
loss of hydrogen ion:
- hyperventilation (loss of CO2)
- utilization of hydrogen ion in metabolism
- loss of hydrogen in vomitus (loss of gastric fluid) and loss into the urine.
- (think of it as shifting the balance of the equation H2CO3 <--> HCO3- + H+
carbonic anhydrase converts CO2+H2O to H2CO3, which is broken down into HCO3- and H+
- therefore, loss of one bicarbonate from the body is equivalent to gain of one H+
- gain of one bicarbonate is loss of one H+
buffer: any substances that reversibly bind to hydrogen ions
- extracellular buffer: Co2/HCO3- system --> keep pH around 7.4
- intracellular buffers: phosphates, proteins

respiratory system (controls CO2)
kidneys (by controlling HCO3-)
- when alkalosis (high pH >7.4) : kdiney excrete HCO3 to gain H+
- when acidosis (pH < 7.4) : kidney produce new HCO3- and add it to the plasma
  - pH is determined by ratio of concentrations of HCO3- to CO2
usually kdineys reabsorb all the filtered HCO3- (80% reabsorption occurs in glomerulus)
- except in the case of alkalosis

H2O and CO2 get converted to H2CO3 by carobnic anhydrase in tubular epithelial cells
H2CO3 get broken down itno H+ and HCO-
HCO- diffuse into the intersittial fluid (gain of one HCO3-)
H+ diffuse inot tubular lumen and combines with filtered HCO3- , producing H2O and CO2
H2O and CO2 diffuse into the epithelai cells, process repeat.
netgain: one HCO3-

same process as above, except that this time, the hydrogen ion diffused into the tubular lumen combines with nonbicarbonate buffer (such as HPO4^2-.
- so body gains HCO3- from H2CO3 and didn't use up a HCO3- to accept the hydrogen ion.
filtered glutamine diffuses into epithelial cells along with sodium and get converted into NH4+ and HCO3-
- HCO3- diffuse into the interstitual fluid
- NH4+ diffuse into the tubular lumen (antitransporter for NH4+ and NA+)
  - (so also loss of hydrogens)

Monday, January 1, 2012
Renal: Potassium and hydrogen regulation