Urinary System Flashcards
State the seven major functions of the
kidneys.
- Excretion of metabolic waste products
* Urea, creatinine, bilirubin, hydrogen - Excretion of foreign chemicals
* Drugs, toxins, pesticides, food additives - Secretion, metabolism & excretion of hormones
* Erythropoetin
* 1,25 dihydroxycholecalciferol (Vitamin D)
* Renin
* Most peptide hormones - Regulation of acid-base balance
- Gluconeogenesis
* Glucose synthesis from amino acids - Control of arterial pressure
- Regulation of water & electrolyte excretion
Describe the mechanism of moving urine from kidneys into bladder
Urine formed in the nephron collects into the renal pelvis of the kidney .
Urine then travels down the ureter due to gravity but
aided by peristalsis into the bladder, acheived by smooth muscle.the pacemaker activity of the smooth muscle in the ureters also contain
mechanosensitive channels that increase the rate of depolarization when they encounter stretch.
Micturition Reflex (At Rest)
Internal sphincter is
contracted (passively)
* External sphincter is
contracted (skeletal
muscle)
* Toxic discharge of
somatic motor neuron
* Higher CNS input, also
Micturation
Stretch receptors on
bladder send afferent
signal to the spinal cord;
leads to:
* Parasympathetic neurons
activating bladder muscle
* Bladder smooth
muscle contracts,
pulling internal
sphincter open
* Inhibition of somatic motor
neuron
* External sphincter
relaxed
* Can be inhibited by CNS
Explain the process of urination and the micturition reflex
the bladder is innervated by the sympathetic nervous system only to control blood flow to the bladder.
The parasympathetic nervous system innervates the bladder, the neck, and the sphincters (Md: somatic motor neuron]
At rest, the internal sphincter is contracted passively and the external sphincter is contracted through skeletal muscle by toxic APs down the somatic motor neuron.
During the micturition reflex, stretch receptors on the bladder send afferent signals to the spinal cord.
This will lead to parasympathetic motor neurons activating the bladder smooth muscle, causing contraction + opening of the internal sphincter.
It also leads to inhibition of the somatic motor neuron l
pudendal) to relax the external sphincter
Excretion
Filtration-Reabsorption+Secretion
Filtration
- Somewhat variable
- Not selective (except for proteins)
- Averages 20% of renal plasma flow
- Takes place at
glomerulus - Substances must
cross filtration
membrane - Glomerular filtrate
composition is about
the same as plasma,
except for large
proteins
Reabsorption
Highly variable and selective
* Most electrolytes (e.g. Na+, K+, Cl-) and nutritional
substances (e.g. glucose) are almost completely
reabsorbed
* Most waste products (e.g. urea) are poorly reabsorbed
Secretion
- Highly variable and selective
- Important for rapidly excreting some waste products (e.g. H+),
foreign substances (including drugs), and toxins
Define filtration , reabsorption,
and secretion .
Filtration is the process the Bowman’s capsule uses to remove waste from the blood. It is somewhat variable and not selective, except concerning proteins. ~ 20% of renal plasma flow is filtered, the remaining 80% continues to the peritubular capillaries.
Reabsorption is the process of putting some components of solute in the nephron back into the blood. It uses energy that is highly variable and selective. Most electrolytes Na+,k+, and nutrients (glucose) as almost completely reabsorbed.
Most waste products are not reabsorbed at all.
Secretion is the process of components of blood being put into the nephron. It is highly selective and variable and uses energy for action. Secretion is important for rapidly excreting waste products.
Glomerular Filtration Rate (GFR)
GFR = 125 ml/min = 180 liters/day
* Plasma volume is filtered 60 times per day
* Filtration fraction (GFR / Renal Plasma
Flow)
= 0.2 (i.e. 20% of plasma is filtered)
Filtration Coefficient of
Glomerular Capillaries
- Kf describes permeability
- In glomerular capillaries, Kf = GFR/NFP
- Normally not highly variable
Using normal values:
Kf = 125ml/min / 10 mmHg
= 12.5ml/min/mmHg
Bowman’s Capsule
Hydrostatic Pressure (PBC)
Normally changes as a function of GFR
* Affected by
* Tubular Obstruction
* Kidney stones
* Tubular necrosis
* Urinary tract obstruction
* Prostrate hypertrophy
* Cancer
Glomerular Capillary Osmotic
Pressure (Pi G)
Affected by
* Arterial plasma oncotic pressure (Pi A)
* increase in Pi A causes increase Pi G
* Filtration fraction (FF)
* increase in FF causes increase Pi G
Glomerular Hydrostatic Pressure (PG)
- Influenced by
- arterial pressure (effect is buffered by
autoregulation) - afferent arteriolar resistance
- efferent arteriolar resistance
- PG is GFR determinant most subject
to physiological control
Renal Blood Flow (RBF)
Kidneys get ~22% of
CO
* To maintain GFR
* Much more than O2 or
nutrient demand
* Kidneys consume ~2X
as much O2 as brain
(per gram weight)
Determinants of RBF
RBF = P / R
* P = renal artery pressure – renal vein pressure
* R = total renal vascular resistance
* Sum of resistances of all renal vessels
Control of GFR and RBF
Neuralhormonal/Paracrine
1. Sympathetic Nervous System
2. Angiotensin II
3. Endothelin
4. Prostaglandins
5. Endothelial-Derived Nitric Oxide
* Local/intrinsic
Sympathetic Nervous System/
catecholamines
(strong innervation)
Increase in RA + Increase RE -> decrease in GFR & decrease in RBF
Endothelin
(released by damaged vessels)
Increase in RA + Increase RE –> decrease in GFR & decrease in RBF
Angiotensin II
(helps prevent GFR)
Increase RE <——-> GFR & decrease in RBF
Prostaglandins/Bradykinin
Decrease in RA + Decrease RE -> Increase in GFR & Increase in RBF
Endothelial-Derived Nitric Oxide (EDRF)
Decrease in RA + Decrease RE -> Increase in GFR & Increase in RBF
Local Control of GFR and RBF
Autoregulation of GFR and RBF
* Myogenic regulation
* Macula densa feedback (tubuloglomerular)
* Angiotensin II
Reabsorption Rate
Filtration Rate – Excretion Rate
Filtration Rate
GFR x Plasma Concentration
Excretion rate
Urine Concentration s x V
(V = urine flow rate)
Transport Maximum (Tm)
Maximum rate of reabsorption or secretion
* Some substances have this due to saturation of
carriers, limited ATP, etc.
* When Tm of reabsorption is reached for all
nephrons, further increases in tubular load are
not reabsorbed and are excreted
Renal Threshold
Tubular load at which Tm is exceeded in some
nephrons
* This is not exactly the same as the Tm of the
whole kidney because some nephrons have
lower transport maximums than others
Loop of Henle
Thin descending limb
* Very permeable to H2O
* Thick ascending limb
* Reabsorbs ~25% filtered
loads of Na+, Cl-, K+
* Also reabsorbs Ca++,
HCO3-, Mg++
* Secretes H+
* Impermeable to H2O
Early Distal Tubule
Like thick loop
* Not permeable to H2O
* Reabsorbs ~5% filtered
loads of Na+
* Also reabsorbs Cl-,
Ca++, Mg++
* Impermeable to H2O
* Contains macula densa
Late Distal Tubule &
Cortical Collecting Duct
Reabsorbs H2O (w/ADH)
* Principle cells
* Absorb Na+ and Cl-
* Secrete K+
* Type A intercalated cells
* Absorb K+ and HCO3-
* Secrete H+ and Cl-
* Type B intercalated cells
(not shown)
* Secrete K+ and HCO3-
* Reabsorb H+ and Cl-
Medullary Collecting Duct
Reabsorbs H2O
(w/ADH)
* Reabsorbs Na+, Cl-,
HCO3-, and urea
* Secretes H+
Regulation of Tubule Reabsorption
Glomerulotubular Balance
* Peritubular Capillary Starling Forces
* Arterial Pressure (pressure natriuresis and
pressure diuresis)
* Hormones
* Aldosterone
* Angiotensin II
* Antidiuretic hormone (ADH)
* Natriuretic hormones (ANF/ANP)
* Parathyroid hormone (PTH)
* Sympathetic Nervous System
Peritubular Capillary Reabsorption
Reabsorption = Net Reabsorptive Pressure X Kf
= 10 mmHg X 12.4 ml/min/mmHg
= 124 ml/min
Aldosterone – Collecting Duct
Increases Na+ reabsorption (and H2O)
* Increases K+ and H+ secretion
Increase aldosterone secretion
Angiotensin II
* Increased K+
* ACTH
Decrease aldosterone secretion
Atrial natriuretic factor (ANF) (aka ANP)
* Increased Na+ concentration/osmolarity
Angiotensin II
Increases Na+ reabsorption (and H2O)
* Proximal tubule, thick ascending limb, collecting
tubule
* Increases H+ secretion
* Stimulates aldosterone secretion
* Constricts efferent arterioles
* decreases peritubular capillary hydrostatic
pressure
* increases filtration fraction
- which increases peritubular colloid osmotic pressure
Angiotensin II Blockade
Decreases Na+ reabsorption (and H2O)
* Proximal tubule, thick ascending limb, collecting tubule
* Decreases MAP
* Medications
* ACE inhibitors (captopril, benazipril, ramipril)
* Ang II antagonists (losartan, candesartin, irbesartan)
* Renin inhibitors (aliskirin)
* Effects
* Decrease aldosterone
* Directly inhibit Na+ reabsorption
* Decrease efferent arteriolar resistance
All lead to natriuresis, diuresis, and decreased BP
Antidiuretic Hormone (ADH/AVP)
Increases H2O reabsorption
* Target cells are distal tubule/collecting
duct
* Regulates ECF osmolarity
* Allows differential control of water and
solutes
Stimulus: increased
osmolarity
* Receptors:
osmoreceptors
(hypothalamus)
Also integrating center
* Output signal: ADH
Atrial Natriuretic Peptide
Stimulus: Atrial stretch
* Detected by myocardial cells
* ANP (or atrial natriuretic factor, ANF)
released by myocardium
* Peptide hormone
* Half-life of 2-3 minutes
* Targets: brain, adrenal medulla, kidney
ANP Effects on Kidneys
Increases GFR
* Dilates afferent arteriole and constricts efferent
* Increases vasa recta flow
* Decreases Na+ and H2O reabsorption
* Less Na+ channels in apical membrane
* Decreases sympathetic activity
* Inhibits renin
Has other effects elsewhere in body
All lower blood volume/pressure
Parathyroid Hormone (PTH)
- Works on thick
ascending
limb/distal tubule - cAMP GPCR
Sympathetic Nervous System
Regulation of Absorption
Decreases Na+ and H2O excretion
* Causes constriction of arterioles
* Lowers GFR
* Increases Na+ reabsorption along tubule
* Increases renin & angiotensin II
Clearance
Clearance describes the rate at which
substances are removed (cleared) from
the plasma.
* Renal clearance of a substance is the
volume of plasma completely cleared of a
substance per min by the kidneys.
C s =Urine [s] X Urine Flow Rate / Plasma [s]
Effects of Countercurrent
Multiplier
More solute than water is added to the renal
medulla
* solutes are “trapped” in the renal medulla
* Fluid in the ascending loop is diluted
* Most of the water reabsorption occurs in the cortex
* in the proximal tubule and in the distal convoluted
tubule, rather than in the medulla
* Horizontal gradient of solute concentration
established by the active pumping of NaCl is
“multiplied” by countercurrent flow of fluid.
Reasons for Concentrated Medulla
Active transport of Na+, Cl-, K+ and other
ions from thick ascending loop of Henle
into medullary interstitial fluid
* Active transport of ions from medullary
collecting ducts into interstitial fluid
* Passive diffusion of urea from medullary
collecting ducts into interstitial fluid
* Diffusion of only small amounts of water
into medullary interstitial fluid
Urea Handling
Urea is passively reabsorbed
in proximal tubule (~ 50% of
filtered load)
* In the presence of ADH, water
is reabsorbed in distal and
collecting tubules,
concentrating urea in these
parts of the nephron
* The inner medullary collecting
tubule is highly permeable to
urea, which diffuses into the
medullary interstitial fluid
* ADH increases urea
permeability of medullary
collecting tubule by activating
urea transporters (UT-1)
ADH
Stimulus for release
* Increased osmolarity
* Decreased blood volume
(cardiopulmonary reflexes)
* Decreased blood pressure
(baroreceptor reflexes)
* Angiotensin II
* These things also stimulate
thirst
* Opposite factors decrease
release
Guyton, 13th Ed., Fig. 29-10
Mechanisms of H+ Regulation
Body fluid chemical buffers (rapid but temporary)
* bicarbonate - ammonia
* proteins - phosphate
2. Lungs
3. Kidneys
Body fluid chemical buffers (rapid but temporary)
- bicarbonate - ammonia
- proteins - phosphate
Bicarbonate
most important ECF buffer
H2O + CO2 <–>H2CO3 <—>H+ + HCO3 -
Phosphate
important renal tubular buffer
HPO4– + H+ <—>H2PO 4 -
Ammonia
important renal tubular buffer
NH3 + H+<—> NH4+
Proteins
important intracellular buffers
H+ + Hb <—> HHb
Lungs
(rapid, eliminates CO2)
Increase H+-> Increase ventilation -> Increase loss in CO2
Kidneys
(slow, powerful); eliminates non-volatile
acids
* secrete H+
* reabsorb HCO3-
* generate new HCO3-
Acidosis
pH < 7.4
- metabolic: decrease HCO3 -
- respiratory: increase PCO2
- increased H+ excretion
- increased HCO3- reabsorption
- production of new HCO3-
Alkalosis
pH > 7.4
- metabolic: Increase HCO3 -
- respiratory: Decrease PCO2
- decreased H+ excretion
- decreased HCO3- reabsorption
- loss of HCO3- in urine
ANP Effects on Other Tissues (Hypothalamus)
Less vasopressin released
ANP Effects on Other Tissues (Medulla Oblongata)
Decreases sympathetic output
ANP Effects on Other Tissues (Adrenal Cortex)
Less aldosterone secreted
Factors that Decrease Renal Excretion/
Increase BP
- Angiotensin II
- Aldosterone
- Sympathetic Activation
Renin Angiotensin System
Increases blood pressure by several
mechanisms
* Renin released in response to ↓ BP
* Directly causes granular cells of afferent arteriole to
produce renin
* ↓BP causes ↓GFR, which causes ↓NaCl transport.
Macula densa sense ↓NaCl and release paracrines
that cause granular cells to release renin
* ↓BP activates medulla oblongata to increase
sympathetic activity, which causes granular cells to
release renin
Renin is released into blood
* It is an enzyme that converts
angiotensinogen (secreted into blood by the
liver) into angiotensin I (ANG I)
* ANG I in the blood is converted to ANG II
by angiotensin converting enzyme (ACE),
which is produced by vascular endothelium
Angiotensin II (ANG II)
Increases blood volume and pressure
* Peptide hormone
* Dissolved in plasma
* Half life ~1 min
* Receptor: AT receptors
* AT-1: GPCR, coupled to Gq/11 and Gi/o
Effects of Angiotensin II (Kidneys)
Causes ↑ Na+ absorption in proximal tubule
* Receptor is GPCR that results in ↑Na+ pumps
and channels
increase volume (and BP) and maintain
osmolarity
Effects of Angiotensin II (Adrenal cortex)
- Causes release of aldosterone
- ↑ Na+ absorption in distal nephron
increase volume (and BP) and maintain
osmolarity
Effects of Angiotensin II (Hypothalamus)
- Increases thirst
- Increases ADH release
- Increases volume
- Increases BP
Effects of Angiotensin II (Arterioles)
Directly causes vasoconstriction (lead to increased blood pressure
)
Effects of Angiotensin II (Medulla oblongata)
Increases sympathetic response (lead to increased blood pressure
)
