BIOL 320 1st Edition Lecture 23Outline of Last Lecture I. J UrethraII. Developmental Aspects of Renal SystemIII. Body Water ContentIV. Fluid CompartmentsV. Composition of Body FluidsVI. Water Balance & ECF OsmolalityVII. Regulation of Water IntakeVIII. Regulation of Water OutputIX. Disorders of Water BalanceX. EdemaXI. Electrolyte BalanceOutline of Current Lecture XII. Sodium Balance RegulationXIII. BaroreceptorsXIV. Blood Pressure HomeostasisXV. Other Hormones with Effects on SodiumXVI. Electrolyte Balance: PotassiumXVII. Calcium RegulationXVIII. Anion RegulationXIX. Acid-Base BalanceXX. Bicarbonate Buffer SystemXXI. Phosphate Buffer SystemXXII. Protein Buffer SystemXXIII. Respiratory Buffer SystemXXIV. Renal pH RegulationXXV. Diagnosis of pH AnomaliesXXVI. Respiratory CompensationXXVII. Renal CompensationXXVIII. Developmental AspectsCurrent LectureSodium Balance Regulation: Aldosterone- -Sodium reabsorptiono --65% proximal tubuleso --25% loop of Henle- -When aldosterone is high all remaining sodium actively reabsorbed- -When tubule permeability is increased with ADH, water follow sodium- -Renin-angiotensin mechanism (JGA) [sympathetic nervous system can also activate this]Baroreceptors- -Pressure diuresis:1. Baroreceptors alert brain of increased blood pressure2. S-ANS impulses to kidneys decrease3. Afferent arterioles dilate4. GFR increases5. Sodium and water output increases6. Blood pressure decreases- -If blood pressure drops…the opposite (1-6).Blood Pressure HomeostasisOther Hormone with Effect on Sodium:- -Estrogen enhances NaCl reabsorb in tubules; water retention; functions to increase fluid (edema) in pregnancy- -Progesterone decreases sodium reabsorb; functions as a diuretic (water & sodium loss)- -Glucocorticoids enhance sodium reabsorb; edemaElectrolyte Balance: Potassium- Usually maintained inside cells- Increases in blood can depolarize cells & damage nerve and muscle function- Kidney filters & secretes potassium- Aldosterone stimulates tubule cells to secrete potassium- Hyperkalemia: too much blood potassium due to renal or adrenal problems, cardiac, muscle, CNS malfunction- Hypokalemia: too little blood potassium due to GI and/or adrenal disordersCalcium Regulation- -Calcium in ECF is important for:1. Neuromuscular function2. Blood clotting3. Membrane permeability, secretions- -Hypocalcemia: excitable, tetany- -Hypercalcemia: muscle/nerve inhibition (arrhythmias)- -Calcium balance controlled by PTH & calcitonin- -PTH: promotes increased blood calcium concentration- -Inhibited by hi/normal blood calcium concentration- -Targets: bones (increase osteoclast activity); kidney (reabsorb calcium); GI (absorb all calcium)- -Calcitonin: in response to increase blood calcium concentration; antagonistic to PTH; not major player in calcium regulationAnion Regulation- -Major anion: Chlorine- -Reabsorbed: under normal pH, 99% chlorine reabsorbed- -During acidosis: fewer chlorine reabsorbedAcid-Base Balance- -Blood pH limits: 7.0-7.8- -Outside these ranges: proteins damaged & cease to function- -Normal blood pH: 7.35-7.45- -Intracellular fluid: 7.0 (carbon dioxide)- -Acids: by-product of metabolism- -Carbonic acid: from carbon dioxide- -Lactic acid: anaerobic metabolism- -Phosphoric acid: protein metabolism- -Organic acids: from carbohydrate & fat metabolism- -Stomach acid: HCl- Concentration of hydrogen ions is regulated sequentially by:o -Chemical buffer systems: rapid, first line of defenseo -Brain stem respiratory centers: within 1-3 minuteso -Renal mechanisms: most potent but takes time (hours, days?) to effect pH changes- Acidosis: pH is too low (less than 7.35)- Alkalosis: pH is too high (greater than 7.45)- -Respiratory acidosis: due to impaired breathing- -Respiratory alkalosis: due to hyperventilation- -Metabolic acidosis: starvation (untreated diabetic…body oxidized fatty acids and amino acids for fuel)- -Metabolic alkalosis: loss of stomach acid (vomiting)Bicarbonate Buffer System- -Mix of H2CO3 (carbonic acid, weak acid) & NaHCO3 (sodium bicarbonate, weak base)- -The only important buffer in both ECF [plasma] (buffers both ICF & ECF)- -pH changes only slightly- -Supply almost limitless (from carbon dioxide respiration)Phosphate Buffer System- -Buffer system commonly in urine & intracellular fluidProtein Buffer System- -Amphoteric (can act as both acid & base) [COOH & NH2]- -Proteins plentiful inside cell; also in plasmaRespiratory Buffer System- CO2 + H20 <--> H2CO3 <--> H+ + HCO3-- -Hypercapnia: elevated carbon dioxide in blood; acidotic; blow off- -Alkalosis: respiratory activity decreases; shallower breathing- -Respiratory system impairment: emphysemaRenal pH Regulation- -Chemical buffers: tie up excess acid/base but cannot remove from body- -Elimination of carbonic acid: via lungs- -Elimination of metabolic acids: via kidneys (lactic, phosphoric, keto, uric acid)- -Mechanisms:1. Reabsorb or generate new bicarb ion2. Excrete bicarb ion- *Losing a bicarb ion = gaining H+*Diagnosis of pH Anomalies- -P(CO2) < 35 mm Hg: respiratory alkalosis- -P(CO2) > 45 mm Hg: respiratory acidosis- -Metabolic: any pH imbalance not caused by abnormal blood concentration of carbon dioxide (checked by bicarbonate ion levels in blood)- -Compensation: respiratory system compensates for metabolic disturbances/problems; kidneys attempt to balance/correct respiratory imbalancesRespiratory Compensation- -For metabolic alkalosis: slow, shallow breathing accumulates CO2- -For metabolic acidosis: increase respiration, lower CO2 levelsRenal Compensation- -For respiratory alkalosis: low CO2 levels, high pH levels; renal compensation indicated by decreased bicarb levels- -For respiratory acidosis: renal compensation indicated by increased bicarb levelsDevelopmental Aspects- -At birth: water content highest- -In youth, buffer problems are typical, due to:1. Low lung volume2. High fluid exchange rate3. High metabolic rate4. High insensible water loss5. Kidneys inefficient in infants- -At puberty: gender differences --> muscle vs. fat differences --> water differences- -With age: homeostatic mechanisms slow- -The elderly: often unresponsive to thirst cues- -Most frequent victims of buffer imbalances: very young &