REGULATION OF WATER &ELECTROLYTES BALANCEby:Husnil Kadri

Biochemistry Departement Medical Faculty Of Andalas University Padang

Maintenance of Blood Pressure Homeostasis

Angiotensin Pathway

Regulation of Water The hypothalamic thirst center is stimulated:By a decline in plasma volume of 10%15%By increases in plasma osmolality of 12%Via baroreceptor input, angiotensin II, and other stimuli

OsmoregulationOsmoreceptors:Increase in plasma osm--> hypothalamus stimulated to release ADH (hypothalamic set point 285 mOsm/L solution)Respond to < 2% change in plasma osmolarity

Regulation of Water Thirst is quenched as soon as we begin to drink waterFeedback signals that inhibit the thirst centers include:Moistening of the mucosa of the mouth and throatActivation of stomach and intestinal stretch receptors

Regulation of Water LossObligatory water losses include:Insensible water losses from lungs and skinWater that accompanies undigested food residues in fecesObligatory water loss reflects the fact that:Kidneys excrete 900-1200 mOsm of solutes to maintain blood homeostasisUrine solutes must be flushed out of the body in water

Regulation of ADH Factors that specifically trigger ADH release include: prolonged fever; excessive sweating, vomiting, or diarrhea; severe blood loss; and traumatic burns.

Regulation of ADH

Disorders of Water Balance: Dehydration

Causes include: hemorrhage, severe burns, prolonged vomiting or diarrhea, profuse sweating, water deprivation, and diuretic abuseSigns and symptoms: cottonmouth, thirst, dry flushed skin, and oliguriaOther consequences include hypovolemic shock and loss of electrolytes

Disorders of Water Balance: EdemaAtypical accumulation of fluid in the interstitial space, leading to tissue swellingCaused by anything that increases flow of fluids out of the bloodstream or hinders their return

EdemaHindered fluid return usually reflects an imbalance in colloid osmotic pressures Hypoproteinemia low levels of plasma proteinsForces fluids out of capillary beds at the arterial endsFluids fail to return at the venous endsResults from protein malnutrition, liver disease, or glomerulonephritis

EdemaBlocked (or surgically removed) lymph vessels:Cause leaked proteins to accumulate in interstitial fluidExert increasing colloid osmotic pressure, which draws fluid from the bloodInterstitial fluid accumulation results in low blood pressure and severely impaired circulation

Electrolyte BalanceElectrolytes are salts, acids, and bases, but electrolyte balance usually refers only to salt balanceSalts enter the body by ingestion and are lost via perspiration, feces, and urine

Sodium in Fluid and Electrolyte Balance

Sodium salts:Account for 90-95% of all solutes in the ECFContribute 280 mOsm of the total 300 mOsm ECF solute concentrationSodium is the single most abundant cation in the ECFSodium is the only cation exerting significant osmotic pressure

Sodium reabsorption is almost always by active transportNa+ enters the tubule cells at the luminal membraneIs actively transported out of the tubules by a Na+-K+ ATPase pumpSodium Reabsorption: Primary Active Transport

From there it moves to peritubular capillaries due to:Low hydrostatic pressureHigh osmotic pressure of the bloodNa+ reabsorption provides the energy and the means for reabsorbing most other solutesSodium Reabsorption: Primary Active Transport

Regulation of Sodium Balance: AldosteroneSodium reabsorption65% of sodium in filtrate is reabsorbed in the proximal tubules 25% is reclaimed in the loops of HenleWhen aldosterone levels are high, all remaining Na+ is actively reabsorbed

Regulation of Sodium Balance: AldosteroneAdrenal cortical cells are directly stimulated to release aldosterone by elevated K+ levels in the ECFAldosterone brings about its effects (diminished urine output and increased blood volume) slowly

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Atrial Natriuretic Peptide (ANP)Reduces blood pressure and blood volume by inhibiting:Events that promote vasoconstrictionNa+ and water retentionIs released in the heart atria as a response to stretch (elevated blood pressure)Has potent diuretic and natriuretic effectsPromotes excretion of sodium and waterInhibits angiotensin II production

Mechanisms and Consequences of ANP Release

Regulatory Site Of Potassium: Cortical Collecting DuctsLess than 15% of filtered K+ is lost to urine regardless of needK+ balance is controlled in the cortical collecting ducts by changing the amount of potassium secreted into filtrateWhen K+ levels are low, the amount of secretion and excretion is kept to a minimum

Influence of AldosteroneAldosterone stimulates potassium ion secretion by principal cellsIn cortical collecting ducts, for each Na+ reabsorbed, a K+ is secreted Increased K+ in the ECF around the adrenal cortex causes:Release of aldosteronePotassium secretion

Potassium Balance

Renal Potassium Handling

Regulation of Calcium and PhosphatePTH promotes increase in calcium levels by targeting:Bones PTH activates osteoclasts to break down bone matrixSmall intestine PTH enhances intestinal absorption of calciumKidneys PTH enhances calcium reabsorption and decreases phosphate reabsorptionCalcium reabsorption and phosphate excretion go hand in hand

Regulation of Calcium and PhosphateFiltered phosphate is actively reabsorbed in the proximal tubulesIn the absence of PTH, phosphate reabsorption is regulated by its transport maximum and excesses are excreted in urineHigh or normal ECF calcium levels inhibit PTH secretionRelease of calcium from bone is inhibitedLarger amounts of calcium are lost in feces and urineMore phosphate is retained

Influence of CalcitoninReleased in response to rising blood calcium levelsCalcitonin is a PTH antagonist, but its contribution to calcium and phosphate homeostasis is minor to negligible

Regulation of AnionsChloride is the major anion accompanying sodium in the ECF99% of chloride is reabsorbed under normal pH conditionsWhen acidosis occurs, fewer chloride ions are reabsorbed Other anions have transport maximums and excesses are excreted in urine

Calcium, phosphate, and magnesium metabolism

Hereditary disorders of tubular transport

Disorders of s odium and w ater m etabolism

Hyponatremia and h ypernatremia

*Reference

Ivkovic, A and Dave, R. Renal review. ppt. 2008Marieb, EN. Fluid, electrolyte, and acid-base balance. ppt. Pearson Education, Inc. 2004Marieb, EN. The urinary system part B. ppt. 2004. Silverthorn, DU. Integrative Physiology II: Fluid and Electrolyte Balance. Chapter 20, part B. ppt. Pearson Education, Inc. 2004