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Nucleus cytoplasm extracellular fluid water Na+ K+ Cl- sugars proteins plasma intracellular fluid 7% 26% 67%

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Presentation on theme: "Nucleus cytoplasm extracellular fluid water Na+ K+ Cl- sugars proteins plasma intracellular fluid 7% 26% 67%"— Presentation transcript:

1 nucleus cytoplasm extracellular fluid water Na+ K+ Cl- sugars proteins plasma intracellular fluid 7% 26% 67%

2 Definitions Solute Solvent Osmosis Osmotic Pressure Osmolarity Hyperosmotic Hypoosmotic

3 Solutes are dissolved particles in solution (any type) Osmotic pressure depends on the number of solutes/unit volume (rather than chemical nature of solutes)

4 As this column rises higher, it will exert increasing pressure. At some point that hydrostatic pressure will reach an equilibrium, at which point no more net water will move across the semi-permeable membrane. This pressure is the ‘osmotic pressure’ of the starting solution on the right. Osmotic flux of water: --which way will the water move? -- Why is there net water flux tothe right?

5 isosmotic Solutes are dissolved particles in solution (any type) (osmotic pressure is equal)

6 Solutes are dissolved particles in solution (any type) hypersmotic (higher osmotic pressure) hyposmotic (lower osmotic pressure)

7 Water always moves from an area of low osmotic pressure to an area of high osmotic pressure Hyposmotic (lower osmotic pressure) Hyperosmotic (higher osmotic pressure) osmotic pressure: the pressure of water to enter, given the solute concentration Osmosis: movement of water from an Area with lower osmotic pressure to Higher osmotic pressure

8 Osmolarity = concentration of solutes in a solution Osmolarity vs. Molarity: 150 mMol sucrose= 150 mOsm sucrose 150 mMol NaCl= 300 mOsm NaCl Osmotic pressures are generally described in osmolar units:

9 Definitions Solute: Solvent: Osmosis: Osmotic Pressure: Osmolarity: Hyperosmotic: Hypoosmotic: Dissolved particles in a solution movement of water from an area with lower osmotic pressure to higher osmotic pressure the pressure of water to enter, given the solute concentration Concentration of solutes in a solution Higher osmotic pressure Lower osmotic pressure What the particles are dissolved in

10 The Mammalian Kidney glomerulus Bowman’s capsule Proximal tubule Loop of Henle Distal tubule Collecting duct To bladder Extracellular Na+ conc. Passive movement of water H2OH2O Active movement of Na+ Na+ HIGH LOW

11 What it actually looks like Bowman’s capsule Distal tubule Proximal tubule Loop of Henle glomerulus Collecting duct

12 Osmotic ImbalanceHypovolemia

13 Baroreceptors in arteries of the heart Causing an increase in secretion and release of VP VP 2 major effects: 1.Vasoconstriction 2.Water retention in kidney

14 Collecting Duct Cell glomerulus Bowman’s capsule Proximal tubule Loop of Henle Distal tubule Collecting duct To bladder Passive movement of water H2OH2O The water pore is a protein called: aquaporin 2 (AQP2)

15 Collecting Duct: nn filtrate to bladder Basal side of cell apical side of cell Lower Na+ Higher Na+ Extracellular space

16 Collecting Duct: nn to bladder Lower Na+ Higher Na+ No Vasopressin: basal aquaporins Aquaporin 2 H2OH2O H2OH2O H2OH2O Add Vasopressin:

17 Collecting Duct: nn to bladder Lower Na+ Higher Na+ basal aquaporins Aquaporin 2 H2OH2O H2OH2O H2OH2O Add Vasopressin:

18 Collecting Duct Cross-Section Cells labeled with fluorescent antibodies made to the water channel

19 nn Collecting Duct:

20

21 Stain for aquaporin 2 (no vasopressin): Collecting Duct:

22 Stain for aquaporin 2 (no vasopressin): Add Vasopressin:

23 Collecting Duct: Stain for aquaporin 2: Add Vasopressin:

24 Collecting Duct:

25 2 major effects of vasopressin: 1.Vasoconstriction 2.Water retention in kidney: Collecting Duct Cell V2 receptor: localized to the kidney VP Gq PLC IP3 DAG Smooth muscle cell In arteries/capillaries V1a receptor: localized to vascular smooth muscle cells V1a receptor V2 receptor

26 Hypovolemia

27 Control of Aldosterone Secretion Renin Secreted in response to low blood pressure Cells in the capillary walls ANGIOTENSIN I ANGIOTENSIN II angiotensin converting enzyme (ACE: secreted by the lungs) IN THE BLOOD ANGIOTENSINOGEN Made in the liver aldosterone Adrenal gland (cortex)

28 glomerulus Bowman’s capsule Proximal tubule Loop of Henle Distal tubule Collecting duct To bladder Extracellu lar Na+ conc. Active movement of Na+ Na+ ALDOSTERONE: Increases uptake of sodium from filtrate -Increases sodium in the blood -Decreases sodium in urine

29 Aldosterone and Angiotensin II production IN THE BLOOD ANGIOTENSINOGEN ANGIOTENSIN I ANGIOTENSIN II angiotensin converting enzyme (ACE: secreted by the lungs) Made in the liver aldosterone Increases Na+ absorbtion in the kidney Renin from glomerulus Induce release of VP Cause vasoconstriction Stimulate drinking

30 REVIEW: hypovolemia Heart baroreceptors cause posterior pituitary to secrete VP –VP increases vasoconstriction –VP increases water pores in the collecting duct, increasing water absorbtion from filtrate Cells in glomerulus secrete renin –  angiotensin II Increases aldosterone Increases vasoconstriction Increases VP Stimulates drinking –  aldosterone Increase sodium retention A Decrease in Blood Pressure:

31 What about an increase in blood pressure? Baroreceptors in heart stop sending releasing signals to SON and PVN Glomerulosa cells produce less renin Under conditions of excessively high blood pressure: –The atria of the heart secrete Atrial Natriuretic Peptide (ANP) –ANP: Shuts down secretion of VP, renin, and ALDO Increases sodium excretion in the urine Increases diuresis (water loss in urine)

32 Osmotic Imbalance

33 Osmoreceptors: -Present in cells in the hypothalamus -when dehydrated, cause secretion of VP from PVN and SON VP 2 major effects: 1.Vasoconstriction 2.Water retention in kidney Neural cells in hypothalamus containing osmoreceptors

34 Vasopressin and Osmolality

35 Angiotensin and Aldosterone? Cells in the capillary walls These cells are also sensitive to osmolality -under low osmolality they secrete renin -under high osmolality the shut down renin secretion

36 Under conditions of high osmolality IN THE BLOOD ANGIOTENSINOGEN LESS ANGIOTENSIN I LESS ANGIOTENSIN II angiotensin converting enzyme (ACE: secreted by the lungs) Made in the liver LESS aldosterone Decreases Na+ absorbtion in the kidney LESS Renin from glomerulus less VP less vasoconstriction less drinking

37 Osmotic Imbalance Review Osmoreceptors in the brain to signal SON and PVN nuclei to increase VP secretion –VP increases water retention in the kidney Glomerular cells decrease secretion of Renin –Decrease Aldosterone secretion –Decrease Angiotensin II levels High blood osmolality causes:

38 Pathophysiology of Osmoregulatory processes Adipsic hypernatremia –Dipsia is thirst, hypernatremia is high salt load –These patients do not have osmoreceptors in the brain, so they don’t respond to hyperosmolality of the blood No osmoreceptors in the brain –No osmoreceptors, no VP secretion in response to cellular dehydration –They need water, but they aren’t thirsty –They do, however, have functional baroreceptors, and respond normally to changes in blood pressure

39 Pathophysiology of Osmoregulatory processes Adipsic hypernatremia –Dipsia is thirst, hypernatremia is high salt load –These patients do not have osmoreceptors in the brain, so they don’t respond to hyperosmolality of the blood –No osmoreceptors, no VP secretion in response to cellular dehydration –They need water, but they aren’t thirsty Diabetes Insipidus –Two types: Neurogenic DI: Nephrogenic DI:

40 Neurogenic Diabetes Insipidus VP is made but not transported VP 1. no VP is secreted 2. Very little water is retained in the collecting duct Treatment with VP can alleviate the problem

41 Nephrogenic Diabetes Insipidus VP Vasopressin is synthesized and secreted normally Collecting Duct Cell But there is a defect in the cellular mechanism that responds to VP

42 Pathophysiology of Osmoregulatory processes Adipsic hypernatremia –Dipsia is thirst, hypernatremia is high salt load –These patients do not have osmoreceptors in the brain, so they don’t respond to hyperosmolality of the blood –No osmoreceptors, no VP secretion in response to cellular dehydration –They need water, but they aren’t thirsty Diabetes Insipidus –Two types: Neurogenic DI: Problem with VP secretion Nephrogenic DI: Problem with VP receptors in collecting duct Malignant hypertension

43 Pathophysiology of Osmoregulatory processes Adipsic hypernatremia –Dipsia is thirst, hypernatremia is high salt load –These patients do not have osmoreceptors in the brain, so they don’t respond to hyperosmolality of the blood –No osmoreceptors, no VP secretion in response to cellular dehydration –They need water, but they aren’t thirsty Diabetes Insipidus –Two types: Neurogenic DI: Problem with VP secretion Nephrogenic DI: Problem with VP receptors in collecting duct Malignant hypertension –Causes a sudden and severe rise in blood pressure –Can lead to blindness, seizure, chest pain, heart failure

44 ABC Hypothalamus Posterior Pituitary


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