1. REGULATION OF ELECTROLYTES
1.1. Bicarbonate(HCO3⁻)
1.1.1. Located in both ICF and ECF
1.1.1.1. Levels are regulated through the kidneys; when there is too much HCO3⁻ present, it is excreted. If more is needed, the kidneys will regenerate and reabsorb HCO3⁻ ions
1.2. Magnesium(Mg+2)
1.2.1. Magnesium is excreted and conserved by the kidneys
1.2.1.1. Vitamin D and the parathyroid hormone are responsible for the increased intestinal absorption
1.2.1.1.1. Mg+2 is important for intracellular metabolism, specifically in the use of ATP
1.3. Sodium(Na+)
1.3.1. Within the nephrons collecting duct, Na+ reabsorbtion is increased by Aldosterone
1.3.1.1. When Na+ is reabsorbed from the kidney tubules, water and chloride are reabsorbed along with it, which leads to the ECF volume being maintained.
1.4. Potassium(K+)
1.4.1. Maintains acid base balance and contributes to intracellular enzyme reactions
1.4.1.1. K+ excretion is increased by Aldosterone in helps to maintain ICF osmolality
1.5. Calcium(Ca2+)
1.5.1. Ca2+ serum levels are increased by the Parathyroid hormone and Calcitonin
1.6. Chloride(Cl−)
1.6.1. Along with the sodium in the kidney's, Cl− is excreted and reabsorbed
1.6.1.1. In RBC's with the exchange of O2 and CO2, Cl− acts as a Buffer
1.7. Phosphate(PO₄⁻)
1.7.1. By increasing renal excretion, serum levels are decreased by the parathyroid hormone
1.7.1.1. PO₄⁻ has a corresponding relationship with calcium: decreased phosphate levels are done by increasing calcium serum levels; when calcium serum decreases, it causes phosphate levels to increase
1.8. Kozier et al., 2014, pp. 1418-1418
2. REGULATION OF ACID-BASE BALANCE
2.1. Renal Regulation
2.1.1. The kidney's are the "ultimate long-term regulators" when it comes to acid base balance
2.1.2. The kidney's maintain Acid-base regulation by excreting or retaining hydrogen and bicarbonate ions
2.1.3. The kidneys reabsorb and regenerate bicarbonate and excrete hydrogen ions
2.1.4. Hydrogen ions are conserved and excess bicarbonate is excreted when the PH rises (alkalosis) and when present hydrogen ions are not sufficient
2.2. Buffers
2.2.1. Prevent significant change by coming together with or releasing hydrogen ions
2.2.1.1. Buffers bind with the hydrogen ions when the bodily fluids become acidic; when excess hydrogen ions are there within the bodily fluids
2.2.2. Buffers release hydrogen ions when bodily fluids become too alkaline; when there isn't enough hydrogen ions in the bodily fluids
2.2.2.1. Bicarbonate (HCO3⁻) and Carbonic Acid (H2CO3) systems are the major buffers in the ECF
2.3. Respiratory Regulation
2.3.1. By eliminating or retaining Carbon dioxide (CO2), the lungs assist in regulating acid-base balance
2.3.2. When C02 is combined with water (H2O), carbonic acid is formed (CO2+H2O=H2C03); this chemical reaction is reversible
2.4. Kozier et al., 2014, pp. 1418-1419
3. Renin
3.1. Renin plays an implortant role in the regulation process of blood pressure and is released from the juxtaglomerular apparatus of the nephrons
3.1.1. Renin breaks down the Angiotensinogen protein from the liver into Angiotensin1
3.1.2. By a converting enzyme in the lungs Angitensin1 converts to Angitensin2
3.1.3. Angitensin2 stimulates the release of Aldosterone from the Adrenal cortex, which causes retention of NA/Water leading to an increase in ECF. Angitensin2 causes the increase in the peripheral vasoconstriction. Both vasoconstriction and ECF, will lead to an increase of blood pressure.
3.2. Lewis et al., 2014, pp. 1270-1271
4. FLUID BALANCES
4.1. Atrial Natriuretic Factor (ANF)
4.1.1. ANF releases from the heart. respond to excess blood volume causes the atrial walls to stretch.
4.1.1.1. ANF promote NA wasting acting as potent diuretic
4.2. Antidiuretic Hormone (ADH)
4.2.1. Antidiuretic Hormone (ADH), causes water regulation from the kidneys.
4.2.2. ADH acts on the collecting ducts of the nephrons and is produced when serum osmolality rises, thus leading to the ducts becoming permeable to water
4.2.3. How ADH regulates water excretion from the kidneys:
4.2.3.1. Increased Blood Osmolality
4.2.3.2. Osmoreceptors in hypothalamus stimulate posterior pituitary to secrete ADH
4.2.3.3. ADH increases distal tubule permeability
4.2.3.4. Increased reabsorption of H2O in the blood
4.2.3.5. Urine output decrease (serum/blood osmolality decrease as the water dilutes body fluids)
4.2.4. Decreased Increased Blood Osmolality
4.2.5. ADH is suppressed
4.2.6. ADH causes distal tubules to become less permeable to water
4.2.7. Decreased reabsorption of H2O in the blood
4.2.8. Urine output increase (serum osmolality returns to normal)