Fluid and Electrolyte Homeostasis

Study Notes

Renal, respiratory, and cardiovascular systems control fluid and electrolyte balance
Renal compensation is slower than respiratory and cardiovascular compensation
Renal/kidneys are controlled by endocrine and neuroendocrine systems
Respiratory and cardiovascular systems are controlled by neural systems
High osmolarity = low water volume → less urine production
Low osmolarity = high water volume → more urine production
Kidneys are the primary route for ion and water excretion

Creates high osmolarity in the interstitial fluid of the medulla
Active transport of Na+, Cl-, and K+ out of the nephron occurs in the thick ascending limb
Necessary for making concentrated urine as filtrate flows through the collecting duct
Pumping ions establishes a gradient for other substances to passively follow
Vasa recta capillaries act as a countercurrent exchanger, removing water from the nephron to prevent medulla dilution
Urea plays a significant role in increasing interstitial osmolarity

Vasopressin (AVP/ADH) controls collecting duct permeability to water in a graded fashion
Increase in vasopressin causes aquaporins to be inserted into apical membranes of collecting duct
Graded effect matches urine concentration to body's water volume needs
As plasma osmolarity increases (from dehydration or solute intake), the body releases more vasopressin to retain water
In the absence of vasopressin, water permeability in the collecting duct is nearly zero

Aldosterone is released in response to low blood pressure by the renin-angiotensin system
Low blood pressure stimulates granular cells in the kidneys to release renin
Renin converts angiotensinogen to angiotensin I, then to angiotensin II (ANG II) by ACE
ANG II stimulates aldosterone secretion and has other effects on blood pressure
Three mechanisms for low blood pressure to initiate renin production: increasing sympathetic activity, granular cells' response to stretch, and low glomerular filtration rate (GFR) causing changes in NaCl transport

Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are released in response to increased blood volume
These peptides enhance Na+ excretion and urinary water loss
They increase glomerular filtration rate (GFR), inhibit tubular reabsorption of NaCl (salt), and inhibit the release of renin, aldosterone, and vasopressin
ANP is released in response to high blood pressure

Potassium homeostasis maintains plasma K+ concentrations within a narrow range
Hyperkalemia (too much potassium) can lead to cardiac arrhythmias
Hypokalemia (too little potassium) can cause muscle weakness, and respiratory muscle failure

Carbon dioxide (CO2) from respiration is a major source of acid
CO2 combines with water to form H+ and bicarbonate (HCO3-) with the assistance of carbonic anhydrase
Buffers, ventilation, and kidneys help maintain pH through compensation of minute-to-minute pH shifts

Respiration is the first response to pH changes in the body
Chemoreceptors in the carotid and aortic bodies monitor changes in pH and stimulate the respiratory control center in the medulla to adjust breathing rate and depth, helping to control CO2 levels in the blood, which in turn affects the pH

Kidneys compensate for pH changes by regulating the secretion and reabsorption of hydrogen (H+) and bicarbonate (HCO3-) ions in the urine
Intercalated cells in the collecting ducts are responsible for fine pH regulation, especially in response to acidosis or alkalosis.