7.6: Water Balance Antidiuretic hormone (ADH): causes the kidneys to increase water reabsorption Regulating ADH: 1.water intake 2.[blood solute] 3.blood.

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Presentation transcript:

7.6: Water Balance Antidiuretic hormone (ADH): causes the kidneys to increase water reabsorption Regulating ADH: 1.water intake 2.[blood solute] 3.blood osmotic pressure and is sensed by osmoreceptors in the hypothalamus 4.hypothalamus cells shrink; nerve message is sent to the pituitary gland to release ADH; initiates sensation of thirst 5.ADH is carried to the kidneys and signals the reabsorption of water 6.This produces a more concentrated urine

Osmotic Pressure (H2O balance – Regulating ADH) high osmotic pressure = when there is little water in blood (dehydrated) … this causes water to rush out of cells to enter bloodstream. A hormone, antidiuretic hormone (ADH), helps regulate the osmotic pressure of bodily fluids by causing the kidneys to increase water reabsorption

Communication between hypothalamus and pituitary gland. * ADH secretion triggers reabsorption of water at the kidney. Animation: Hormonal Communication

behavioural change Osmoreceptors in hypothalamus (brain) -detect osmotic change How? (blood:  water =  solutes = shrinkage of cells in hypothalamus as water leaves)   hormonal change Creates the sensation of thirst ADH (hormone made in hypothalamus, stored in pituitary)  Released to the bloodstream  = drink more =  osmotic pressure ADH to kidneys via blood = increase in water uptake How?  makes the usually impermeable distal tubule and collecting duct permeable to water  water is ‘sucked’ out because of high NaCl concentration in intercellular spaces  = osmoreceptors swell  =  in ADH

Kidneys and Blood Pressure 1. low blood volume and low blood pressure 2.sensed by blood pressure receptors in juxtaglomerular apparatus 3.renin is released to convert angiotensinogen into angiotensin 4.angiotensin constricts blood vessels and simulates release of aldosterone from adrenal gland 5.aldosterone is carried to the kidneys 6.nephrons increase Na+ and H2O reabsorption

 Blood Pressure (Adjusting Blood Volume) a hormone aldosterone, produced in the adrenal glands (located above kidneys), acts on the nephrons to increase Na+ reabsorption.  water =  blood pressure =  O2 to tissues so…  receptors near glomerulus detect blood pressure change  = release renin (enzyme) which converts the plasma protein angiotensinogen into angiotensin (enzyme)  * angiotensin has 2 roles: vasoconstriction (constriction of blood vessels) stimulates the release of aldosterone which increases reabsorption of NaCl/H2O at the nephron   in blood pressure

 pH Balance The pH of our body is 7.3  7.5 Cell respiration releases H+ ions into the blood which decreases pH So… our buffer system: H+ + HCO3-  H2CO3  H2O + CO2 But this removes HCO3- ions so we have to get more of them So… 2 things happen (in different parts of the kidney) to replace the HCO3-

 CO 2 (taken in actively) HCO 3 - (out to blood ) peritubule capillary interstitial fluid CO 2 + H 2 O  HCO H + (makes more bicarbonate – sends it back to blood) tubule cells  H + + HPO 4 2-  pee H + + NH 3  pee (the H + ions combine with either phosphate or ammonia – flushed out in filtrate) lumen of tubule Section 7.6, pp. 356, #1-8

Kidney Disease Diabetes Insipidus kidneys don't concentrate urine well Symptoms frequent urination strong thirst response Causes inadequate production of ________. may be caused by head injury or brain tumours. Medication containing lithium Treatment: drink large volumes of water

Diabetes Mellitus islet cells of the pancreas produce little or no insulin Symptoms frequent urination extreme thirst lack of energy vision problems Treatment insulin replacement therapy oral hypoglycemic medication Blood Sugar Animation: Blood Sugar Regulation in Diabetics

Bright's Disease (Nephritis) grouping of diseases characterized by the inflammation of the nephrons. One type of nephritis changes the permeability of the glomerulus allowing proteins to pass into the nephron. This causes an increase in urine production. Kidney Stones caused by the precipitation of mineral solutes from the blood sharp stones can damage tissues Extracorporeal shock-wave lithotripsy (ESWL) breaks stones into smaller fragments that can be voided through the excretory system

Diabetes Mellitus  inadequate secretion of insulin  blood sugar levels rise  you pee out lots of glucose  this messes up the osmotic pressure and more water is lost = lots of peeing  must drink a lot Diabetes Insipidu s  destruction of ADH producing cells in the hypothalamus (not able to control water reabsorption)  urine output increases  you must drink a lot Bright’s Disease  “inflammation of the nephron” = altered permeability  lots of characteristics  start peeing out large molecules like proteins  proteins in tubule = osmotic issues = lots more peeing Kidney Stones  precipitation of mineral solutes from the blood  Ouch!  some can be destroyed by ultrasound

Dialysis Technology  the exchange of substances across a semipermeable membrane haeomodialysis  a tube is connected to a vein and blood is removed from the bodyhaeomodialysis  the blood goes into a dialysis machine (in the tube) and passes through various environments(solutions) that remove toxins from the blood  essentially a “man made” kidney.

peritoneal dialysis  pump dialysis fluids into abdominal cavity (~2 L)peritoneal dialysis  the selectively permeable membranes of the cavity allow toxins to go into the fluid  fluid is removed and new fluid pumped in wastes diffuse from the plasma into the peritoneum and is filtered into the dialysis fluid accumulated wastes are drained off and replaced several times a day performed at home (2-6 hours) neither provide the hormones that kidneys do so they have to be injected

Kidney Transplant 85 % successful new kidney is placed lower in the pelvis and attached to blood vessels and ureter old kidney is not removed patient must receive immunosuppressant drugs forever Section 7.7, pp. 362, #1-10 Review: pp. 367, #1-8; pp. 368, #1-13, 15, 17