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Renal Countercurrent Multiplier System and Sodium Regulation - Prof. Douglas N. Ishii, Study notes of Biology

The renal countercurrent multiplier system, which concentrates solutes in urine, and the regulation of sodium in the body. The role of isosmotic, hypoosmotic, and hyperosmotic fluids, the distribution of ion pumps and aquaporins, and the function of the vasa recta. Additionally, it discusses the regulation of sodium levels through the actions of antidiuretic hormone (adh), mineralocorticoids, and the renin-angiotensin system.

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2011/2012

Uploaded on 05/26/2012

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Download Renal Countercurrent Multiplier System and Sodium Regulation - Prof. Douglas N. Ishii and more Study notes Biology in PDF only on Docsity! 1 May The Countercurrent Multiplier System Concentrates Solutes in Urine Terms: isosmotic (300 mOsm); hypoosmotic; hyperosmotic Example of countercurrent exchange system: A hot water pipe flowing to left. Closely adjacent and parallel is a cold water pipe flowing to the right. The hot water will warm the cold water by countercurrent heat exchange Renal countercurrent multiplier system The descending proximal and ascending distal tubules in the loop of Henle is a countercurrent osmotic exchange system The solute becomes hyperosmotic (multiplied) in the interstitial fluid of the kidney medulla This system is cleverly controlled simply by the distribution of ion pumps and aquaporins along the tubules and ducts Figure 14 – 18 Consider the long loop of the juxtamedullary nephrons ADH and aquaporins H2O flows downhill to hyperosmolar gradient in medullary interstitial fluid to vasa recta Note: Net water flux out of descending tubule until mOsm gradient becomes equal in nearby interstitial fluid to that in descending tubule Water flows downhill into interstitial fluid from the descending proximal tubule, “multiplying” solutes from 300 to 1400 mOsm at the hairpin. Pumping Na+ and Cl- out of the ascending tubule (low aquapoins) reduces mOsm to 100 mOsm at the distal convoluted tubule Figure 14 – 19 The vasa recta follows the descending and ascending limbs of the tubules in the loop of Henle in the renal medulla Interstitial fluid and solutes enter passively. Twice as much flow exits as enters the vasa recta The geometry of the vasa recta parallels the renal countercurrent multiplier system, assuring that the blood in these vessels does not “wash out” the osmotic gradient Renal Sodium Regulation Despite a wide range of Na+ intake, its amount in the body is normally tightly regulated in a narrow range The amount of Na+ excreted equals Amount filtered by GFR Less amount reabsorbed from tubules Na+ is pumped out of cells (low in intracellular fluid comprising 67% water volume) Na+ comprises 90% of solutes in extracellular fluid Na+ levels regulate extracellular volume and blood pressure Baroreceptors responsive to blood pressure and renin regulate Na+ reabsorption and extracellular volume Figure 14 – 21 A reduction in plasma volume reduces GFR and amount of Na+ and water excreted Baroreceptor activation of sympathetic nerves constricts renal afferent arterioles (smooth muscles), reducing GFR Figure 14 – 22 Renin and angiotensin system regulating Na+ reabsorption, plasma volume and blood pressure Increased synthesis of Na+/K+ ATPase in distal tubule and cortical collecting ducts Figure 14 – 23 Baroreceptors control renin release as well as GFR Tubule cells release paracrines Figure 14 – 27 Severe sweating reflex to reduce water and Na+ loss. Recruits baroreceptor, osmoreceptor, renin and ADH pathways Sweat is hypoosmotic Regulating of Water and NaCl Intake Ingestion must replace the daily loss of water and Na+ Survival without water is 10 days <50° F, or 5 days at 100° F Loss of 2L will decrease body performance (hyperosmolarity) Thirst is stimulated by Increased osmolarity Decreased extracellular fluid volume Activation of osmoreceptors and baroreceptors Dryness of mouth and throat Salt appetite Average USA consumption 10 – 15 g/day Recommendation: ingest <3.8 g NaCl/day to reduce risk of hypertension Regulation of Potassium Levels Intracellular: K+ is the most abundant ion Extracellular: K+ is critical for nerve, muscle, and cardiac function Hypokalemia: Abnormally low K+ concentration Hyperkalemia: Abnormally high K+ concentration K+ excreted = (ingested – loss in sweat – loss in feces – amount secreted in tubules) Recall the mechanism for tubular epithelial cell Na+/K+ ATPase. Most of K+ in GFR filtrate is reabsorbed from the proximal tubules Figure 14 – 29: Potassium regulation Most K+ reabsorbed Figure 14 – 14 Almost all K+ is reabsorbed in the proximal tubule But, in the collecting duct, K+ can be secreted into the tubule. The Na+/K+ ATPase controls how much K+ is excreted. K+ secretion is linked to Na+ reabsorption A high K+ diet increases the exchange of K+ for Na+ at the Na+/K+ ATPase. It also increases aldosterone production Figure 14 – 31 Summary K+ effect on the aldosterone pathway in collecting duct High dietary K+ Increases Na+/K+ exchange at the Na+/K+ ATPase Stimulates greater aldosterone secretion to increase Na+/K+ ATPase production Diseases: Abnormal Potassium Levels Primary aldosteronism (Conn’s syndrome): Adenoma of adrenal gland increasing aldosterone production Hypernatremia and hypokalemia Hypervolemia and hypertension Low renin and angiotensin-II levels Treatment: Unilateral adrenalectomy Cushing’s disease: Excess glucocorticoid (cortisol) production
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