Ion and Water Balance Flashcards
What are the three homeostatic processes?
Osmotic Regulation: Water
Ionic regulation: Ions
Nitrogen excretion: Excretion
What are the strategies to cope with ionic & osmotic challenges
Ionoconformer: exert little control over the solute profile within the extracellular space (marine)
Ionoregulator: control ion profile of extracellular space = use active mechanisms
Osmoconformer: internal and external osmolarity are similar
Osmoregulator: osmolarity is constant regardless of external environment
What is osmolarity?
Osmolarity: indication of the total solute concentration. Measure of the total # of solute particles per unit volume.
What is Tonicity? What are the types of tonicity?
Tonicity: The ability of a solution to cause a cell to shrink or swell. Depends of non-penetrating solutions
Isotonic: happy cells
Hypertonic: cells shrink
Hypotonic: cells burst
What is Dietary Water? Metabolic Water?
Dietary: water performed in plant and animal tissues
Metabolic: water generated as a result of oxidative phosphorylation
How do Animals compensate for ion and water movements?
By active transport of ions.
Primary Osmoregulatory epithelium of vertebrates are gills, kidney, and digestive system
How do Sharks maintain osmolarity?
Shark blood contains high levels of urea and TMAO (Trimethylamine oxide)
Maintains blood osmolarity slightly higher than seawater
Gill has specializations to reduce permeability to urea. Sharks gain H2O passively and use urea as a somolyte to increase osmolarity
Using Urea alone would be toxic, needs TMAO
How to Marine mammals differ from Terrestrial mammals? Desert?
Marine Mammals: Do not drink sea water, hyperosmotic (similar to desert)
Terrestrial Mammals: replace lost water through eating and drinking
Desert Mammals: Have little access to freshwater and has efficient kidneys
Can produce concentrated urine to conserve water
What epithelia are involved with ion and water balance? What else are they involved with?
Gills and Kidneys are also involved in the excretion of nitrogenous waste.
Protein catabolism (breakdown) generates ammonia (NH3)
What forms is Amino Acid breakdown is excreted as?
Ammonia, Urea, Uric Acid
What do Mammals produce when dehydrated? Alligators?
Mammals: Dehydrated = produce Uric Acid when = gout
Alligators: Hydrated = produce NH4HCO3 (Ammonium Bicarbonate) Dehydrated = produce Uric Acid
High Uric Acid can lead to gout in animals that dont normally excrete it
Summary of Ammonia
Aquatic Animals avoid ammonia poisoning by dissolving it in large amounts of H2O
Diffuses across gill epithelium/permeable membrated bathed by H2O
Summary of Urea
Urea is soluable in H2O and moderately toxic
Can accumulate Higher levels in tissues w/o damage
excreted in concentrated form and requires energy (pee)
Summary of Uric Acid
Uric Acid is ALMOST insoluble in water
In Cloaca, uric acid joins with ions and precipitates out. Little H2O loss
Nontoxic if doesn’t accumulate, 15 rxn each catalyzed by enzyme = lots of energy to cause rxns.
What are the Functions of the Kidney?
Ion Balance
Osmotic Balance
Blood pressure: a change in blood volume = change in BP
pH Balance: H+
Excretion: helps detoxify
Hormone production: Erythropoietin Calcitriol, Adrenal glands
Gluconeogenesis: making glucose form non-carb stuff (amino acids)
How do Kidneys make glucose via gluconeogenesis
Amino Acids involved: Lactate, Glutamine, Glycerol, Alanine
Catecholamines = stimulus for gluconeogenesis
Renal Medulla: enzymes that help break down glycogen
Renal Cortex: enzymes that make glucose from non-carb
What is the kidney structure?
Crescent shaped with the cortex and medulla
Cortex: Bowman’s capsule, Proximal Tubule, Distal Tubule
Medulla: Collecting Duct, Loop of Henle
What is the Nephron? Nephron Vasculature?
Nephron: functional unit of the kidney, tubular system
Nephron Vasculature:
Afferent Arteriole = Leads to glomerulus
Glomerulus = Twisted ball of Capillaries (little ball)
Efferent arteriole = leads away from glomerulus
Peritubular Capillaries =
Vasa recta =deeper
Explain the juxtaglomerular apparatus
proximal convoluted tuble cells have mirovilli
Juxtaglomerular Apparatus: regulate BP in Kidney
- Jux cells: cells of afferent and efferent
arterioles have modified smooth muscle fibers
Principal Cells: receptor proteins for antidiuretic hormone (ADH) and Aldosterone (on distal convoluted tubule)
Explain Juxtaglomerular Complex
Juxtaglomerular Complex: endocrine structure that secretes hormones and renin
- Hormone/Erythropoietin = released by jux
cells. Goes to red bone marrow to make RBC
- Renin = Enzyme released when BP is low
Macula densa sense NaCl flow change
What are the 4 processes of Urine production?
Filtration
Reabsorption
Secretion
Excretion
Where is Filtration? Explain it
Filtration: produces protein free solution similar to blood plasma
- passive through hydrostatic pressure. Forces water through membrane pores
- proteins and RBC are not filtered
- RBC whole in urine = kidney failure
- RBC lysed = organ failure other than kidney
Filtration at Glomerulus?
- Glomerular capillaries = very leaky
- Podocytes = foot proccesses form filtration structure
- Mesangial cells = control BP & Filtration within glomerulus
What is Filtration Pressure and what are the components?
Filtration Pressure: governed by balance btwn:
Glomerular Hydrostatic Pressure: BP seen @ A arteriole = favors
Capsular Hydrostatic Pressure: fluid within tubular system = opposes filtration
Colloid Osmotic Pressure: bc of proteins (albumin) = opposes filtration = draws fluid back to capillaries.
GHP-CHP-COP=Filtration pressure
How do you regulate Glomerular filtration?
GFR = glomerular filtration rate
regulate GFR by changing diameter of the afferent arteriole
radius of EFFERENT arteriole decreases, GFR increase
If afferent arteriola constricts = GFR Decreases
- INCREASE radius @ A = INCREASE GFR
- DECREASE radius @ A = DECREASE GFR
- INCREASE radius @ E = DECREASE GFR
- DECREASE radius @ E = INCREASE GFR
What is the control of GFR?
GFR= automatically maintained
- Autoregulation = when BP increases at afferent arteriole. Maintains GFR despite BP and blood flow changes (Myogenic and Tubuloglomerular mechanisms)
- Hormonal regulation =
Angiotensin II = potent vasoconstrictor
Natriuretic peptides - Automatic regulation (by sympathetic division of ANS)
Kidney blood vessels supplied by sympathetic ANS fibers release norepinephrine = vasoconstriction = reduce GFR
How do we automatically constrict the afferent arteriole?
Stretch receptors open allowing sodium to enter and getting a depolarization leading to contraction of smooth muscles.
How is filtration regulated in the Renin Angiotensin System?
- Low BP in the cells sensed by Juxtaglomerular cells -> release Renin
RENIN: enzyme converting Angiotensinogen to Angiotensin I. Liver releases Angiotensinogen
Angiotensin: Converting enzyme converts ANG I to ANGII, released by lungs.
ACE inhibitors lower BP
- ANG II = potent vasoconstrictor
1. Hypothalamus: feeling thirsty
2. Hypothalamus makes ADH
3. Adrenal cortex releases Aldosterone
GFR decreases
How is filtration regulated in ADH?
Stimulus: Low blood volume (detected by baroreceptors), increased blood osmolarity (detected by chemoreceptors from hypothalamus), Angiotensin II (from decrease in BP).
Regulation: Hypothalamus increases nerve signals to posterior pituitary, release ADH into blood.
Outcome: Blood pressure increase, blood osmolarity decreases.
How is filtration regulated in Aldosterone?
Stimulus: Angiotensin II (decrease in BP), Decrease in Na+ blood plasma lvls, Increase K+ blood plasma lvls.
Regulation: Adrenal cortex releases Aldosterone to blood
Outcome: Na+ maintained, K+ decreases, Blood volume and BP maintained by decreasing urine output
How is filtration regulated in Natriuretic Peptides?
Simulus: Blood volumed increased (increase stretch of baroreceptors in atria)
Regulation: Atria releases ANP into blood
Outcome: Peripheral resistance decreases, blood volume decreases, BP decreases.
- leads to vasodilation
- Increase GFR = pee out more H2O,
- inhibit ADH synthesis. Aldosterone Not released
- Don’t feel thirsty.
What does reabsorption look like in kidneys? Glucose? H2O?
- Useful materials recaptured before filtrate leaves kindeys.
- Reabsorption occurs in proximal convoluted tubule.
- Diffusion: small hydrophobic stuff
- Osmosis: water
- Channel-mediated diffusion = facilitated diffusion = ions/ 2ndary active transport = if keeping against gradients
- Carrier mediated transport - Obligatory water reabsorption in the proximal tubule = not regulated by ADH = happens automatically to maintain osmolarity of blood leaving kidneys.
What is the countercurrent mechanism in kidneys?
- Loop of Henle: juxtamedullary nephrons function as countercurrent multiplier. Increasing osmotic gradient as we move deeper towards loop of Henle
- Descending limb = permeable to water, water leaves, increase osmolarity
-Ascending limb = permeable to ions, ions leave, decrease osmolarity
- Deeper = higher osmolarity
What is a buffer?
- Buffer act quickly to temporarily bind to H+
- Do not prevent pH changes but will reduce or minimize them.
What are the Buffer Systems?
Protein Buffer System: proteins (-) charged so they can bind to H+
- Most abundant buffer in ICF and blood plasma
-Hemoglobin in RBC = review CO2 & Hemoglobin
Carbonic Acid-Bicarbonate Buffer System: HCO3- = weak base & H2CO3 = weak acid
- HCO3- = significant anion in ICF and ECF
Phosphate Buffer System: Important regulator of pH in cytosol
- H2PO4- & HPO4 2- = major anions in ICF and minor in ECF
Acidosis v.s. Alkalosis
Acidosis: depression of synaptic transmission in CNS
Alkalosis: overexcitability if CNS and peripheral nerves
Respiratory Acidosis v.s. Respiratory Alkalosis
Respiratory Acidosis: Abnormally high PCO2 in systemic arterial blood
- Inadequate exhalation of CO2 = Hypoventilate
- Emphysema, Pulmonary Edema, Airway obstruction = decrease CO2 movement out
- Kidneys pee out H+
Respiratory Alkalosis: Abnormally low PCO2 in systemic arterial blood
- Causes Hyperventilation
- Pulmonary disease, Stroke, Severe anxiety = Hyperventilation
- O2 deficiency from high altitudes = Hyperventilation
Metabolic Acidosis v.s. Metabolic Alkalosis
Metabolic Acidosis: Too much H+
- loss of HCO3-
- Ketosis: accumulate acids other than carbonic acid
- can hyperventilate
Metabolic Alkalosis: Too little H+
- Nonrespiratory loss of acid (vomiting stomach acids) HCl=stomach acid
- Dehydration
- can hypoventilate, keep in CO2
