Urinary system physiology

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Urinary system physiology


Mechanisms of Urine Formation

The kidneys filter the body’s entire plasma volume 60 times each day

The filtrate:

Contains all plasma components except protein

Loses water, nutrients, and essential ions to become urine

The urine contains metabolic wastes and unneeded substances


Glumerular Filtration

The fluid that is forced out of capillaries into the Bowman’s space is called glumerular filtrate

Similar to blood plasma without the proteins

Tubular reabsorption and secretion

The fluid in the DCT and PCT is called tubular fluid

Differs from the filtrate because substances are moving in and out the tubules

Water conservation

Occur in the collecting duct

The fluid is called urine

Basic processes of urine formation


Reminder - Capillary Beds of the Nephron

Every nephron has two capillary beds

Glomerulus

Peritubular capillaries

Each glomerulus is:

Fed by an afferent arteriole

Drained by an efferent arteriole

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummingshttp://members.aol.com/Bio50/LecNotes/lecnot37.html

Most molecules smaller than 3 nm can pass freely. That includes water, electrolytes, glucose, fatty acids, amino acids, nitrogenous wastes and vitamins


Glomerular Filtration Filtration is a passive process in which hydrostatic pressure

forces fluid and solutes through a membrane

The glomerulus is more efficient than other capillary beds because:

Large surface area of the filtration membrane

filtration membrane is more permeable

Glomerular blood pressure is higher because

Arterioles are high-resistance vessels

Afferent arterioles have larger diameters than efferent arterioles

Higher BP results in higher net filtration pressure


Specials characteristics of glumerular filtration Filtration depends on the balance between hydrostatic pressure

and colloid osmotic pressure on both sides of the capillary wall

Blood hydrostatic pressure (BHP) is much higher in the glomerulus (60 mmHg as compared to 10-15)

Hydrostatic pressure in the capsular space is about 18 mm Hg (compared to about 0 in the interstitial fluid).

This is a result of continuous filtration and the presence of fluid in the space.

The colloid osmotic pressure (COP) of the blood is about the same as elsewhere – 32 mm Hg

The glomerular filtrate is almost protein-free and has no significant COP


Glomerular filtration

Total forces in the renal corpuscle:

Forces that work to move fluid from capillaries into capsular space:

Glomerular capillaries hydrostatic pressure (GHP) – 55-60 mm Hg

Forces that work to move fluid out of capsular space to capillaries:

Blood colloid osmotic pressure (BCOP) – 32 mm Hg

Capsular space hydrostatic pressure (CsHP) – 18 mm Hg

60 out – 18 in – 32 in = 10 mmHg net filtration pressure


Net Filtration PressureFiltration pressure across the filtration membrane is equal to the blood hydrostatic pressure (BHP) minus the colloid osmotic pressure (COP) in the glomerular capillary and minus the capsular pressure (CP).


Glomerular filtration rate (GFR)

Amount of filtrate produced by the two kidneys each minute (~125 ml)

Factors that control GFR:

Total surface area available for filtration

Filtration membrane permeability

Net filtration pressure (NFP)

GFR is usually measured over 24 hr and it is about 180 L/day for males and 150 L/day in females


Regulation of Glomerular Filtration

2 types of mechanisms control the GFR

Renal autoregulation (intrinsic system)

Myogenic mechanism

Tubuloglomerular feedback mechanism

Extrinsic mechanisms

Neural controls (extrinsic system)

Hormonal mechanism (the renin-angiotensin system)


Intrinsic Controls - autoregulation

Renal autoregulation is the ability of the nephron to adjust the blood flow and GFR without external control

Under normal conditions, renal autoregulation maintains a nearly constant glomerular filtration rate

Autoregulation involves two types of control

Flow-dependent tubuloglomerular feedback – senses changes in the juxtaglomerular apparatus

Myogenic – responds to changes in pressure in the renal blood vessels


Tubuluglomerular feedback mechanism The juxtaglomerular apparatus (JGA) monitors the fluid entering

the DCT and adjusts the GFR

Components of the JGA:

The granular/juxtaglumerular (JG) cells – enlarged smooth muscle cells in the afferent arteriole.

They respond to the cells of the macula densa to dilate or constrict the arterioles

Act as mechanoreceptors that sense blood pressure

Can release renin when BP decrease

The macula densa is a patch of ET at the start of the DCT (in some books it said to be in loop of Henle) directly across from the JG cell

Sense NaCl concentration in the tubular fluid


Autoregulation control of GFR

If GFR rises, flow of tubular fluid increases and rate of NaCl reabsorption decreases.

The macula densa sense the change and stimulate the contraction of JG cells

This results in constriction of the afferent arteriole thus reducing GFR


Intrinsic Controls: Myogenic Mechanism

The myogenic mechanism – base on the tendency of smooth muscle to contract when stretches

BP constriction of afferent arterioles

Helps maintain normal GFR

Protects glomeruli from damaging high BP

BP dilation of afferent arterioles

Helps maintain normal GFR


Extrinsic Controls – neural control

When the sympathetic nervous system is at rest:

Renal blood vessels are maximally dilated

Autoregulation mechanisms is controlling

Under stress:

Norepinephrine is released by the sympathetic nervous system

Epinephrine is released by the adrenal medulla

Afferent arterioles constrict and filtration is inhibited

The sympathetic nervous system also stimulates the renin-angiotensin mechanism


Renin-Angiotensin Mechanism – hormonal control

A reduction in afferent arteriole pressure triggers the JG cells release renin

Renin acts on angiotensinogen to release angiotensin I

Angiotensin I is converted to angiotensin II

Angiotensin II:

Causes mean arterial pressure to rise

Stimulates the adrenal cortex to release aldosterone

As a result, both systemic and glomerular hydrostatic pressure rise


Extrinsic Controls: Renin-Angiotensin Mechanism

Triggered when the granular cells of the JGA release renin

angiotensinogen (a plasma globulin)

resin

angiotensin I

angiotensin converting enzyme (ACE)

angiotensin II


Reabsorption and secretion Conversion of the glomerular filtrate to urine

involves the removal and addition of chemicals by tubular reabsorption and secretion

Accomplished via diffusion, osmosis, and carrier-mediated transport

Cells of the PCT reabsorb 60-70% of the filtrate volume

Reabsorbed materials enter the peritubular fluid and diffuse into the preitubular capillaries


Nonreabsorbed Substances

Substances are not reabsorbed if they:

Lack carriers

Are not lipid soluble

Are too large to pass through membrane pores


Nonreabsorbed Substances

A transport maximum (Tm):

Reflects the number of carriers in the renal tubules available

Exists for nearly every substance that is actively reabsorbed

When the carriers are saturated, excess of that substance is excreted


Regulation of Urine Concentration and Volume

Osmolality

The number of solute particles dissolved in 1L of water

Reflects the solution’s ability to cause osmosis

Body fluids are measured in milliosmols (mOsm)

The kidneys keep the solute load of body fluids constant at about 300 mOsm

This is accomplished by the countercurrent mechanism


The loop of Henle and countercurrent multiplication

Countercurrent multiplication –exchange occurs between fluids moving in different directions; the effect of the exchange increased as the fluid movement continues

Between the close ascending and descending limbs of loop

Difference in permeability in two arms:

Thin descending is permeable to water and almost not to solutes

Thick ascending relatively impermeable to both but contains active transport mechanism that pump sodium and chloride ions from tubular fluid to peritubular fluid of the medulla


Countercurrent multiplication Sodium and chloride are pumped out of the thick

ascending limb into the peritubular fluid by co-transport carriers (Na+-K+/2Cl- transporter)

That elevates the osmotic concentration in the peritubular fluid around the thin descending limb

The result is flow of water out of the thin descending limb into the peritubular fluid and increased concentration of solutes in the thin limb

The arrival of highly concentrated solution in the thick limb accelerate the reabsorption of sodium and chloride ions


The countercurrent multiplication:

Creates osmotic gradient in medulla

Facilitates reabsorption of water and solutes before the DCT

Permits passive reabsorption of water from tubular fluid in the collecting system


Osmotic gradient

The kidney has an osmotic gradient from cortex to medulla

The outer layer of the kidney is isotonic with the blood: ~300 milliosmoles/liter

The innermost layer (medulla) is very hypertonic: ~1200 milliosmoles/liter


Solutes and water reabsorbed in the medulla need to be returned into circulation.

Blood enters the vasa recta with osmotic concentration of ~300 mOsm/l

Blood descending in the medulla gradually increases in osmotic concentration because of solute reabsorption (plasma proteins limit osmotic flow out of the blood)

Blood flowing toward the cortex gradually decreases in osmotic concentration mainly because of water flowing into capillaries

Function of the vasa recta


DCT performs final adjustment of urine by active secretion or reabsorption

Tubular cells actively reabsorb Na+ and Cl- .

In the distal part of the DCT reabsorption of sodium ions in exchange to another cation (usually K+)

The ion pumps and Na+ channels are regulated by aldosterone

The DCT is a primary site of calcium ions reabsorption (regulated by PTH and calcitriol)

Reabsorption and secretion at the DCT


The concentration of the urine is adjusted in the collecting ducts

The kidney uses osmosis in the collecting duct to control the concentration and volume of urine

The collecting ducts pass through tissue with a very high osmotic pressure in the medulla.

As the urine passes into the collecting duct it first passes through a region of isotonic osmotic pressure (300 milliosmoles/liter) and then through a region of hypertonic osmotic pressure (up to 1200 milliosmoles/liter)

If the collecting duct has low water permeability the dilute urine in the kidney tubule passes through with little uptake of water

If the collecting duct has high water permeability much of the water will be reabsorbed from the collecting duct into the interstitial fluid


ADH and urine volume The permeability of the wall of the collecting duct varies under the

influence of antidiuretic hormone (ADH).

ADH is released by the posterior pituitary in response to increased osmotic pressure (decreased water or increased solutes in blood).

When ADH reaches the kidney, it increases the permeability of the epithelial linings of the distal convoluted tubule and collecting duct to water, and water moves rapidly out of these segments, eventually into the blood, by osmosis (water is reabsorbed).

Consequently, urine volume falls, and urine concentrates soluble wastes and other substances in minimal water. Concentrated urine minimizes loss of body fluids when dehydration is likely.

If the osmotic pressure of the blood decreases, ADH is not released and water stays in the collecting duct, leaves as part of the urine.


Aldosterone and urine concentration Aldosterone is a steroid secreted by the adrenal cortex

It is secreted when blood sodium falls or if blood potassium rises

It is also secreted if BP drops (indirectly through the release of renin-angiotensin II that promotes aldosterone secretion)

Aldosterone secreted – increased tubular reabsorption of Na+ in exchange for secretion of K+ ions – water follow

Net effect is that the body retains NaCl and water and urine volume reduced

The retention of salt and water help to maintain blood pressure and volume


Atrial natriuretic peptide (ANP) and urine volume Secreted from the atrial myocardium in response to high

BP

Has 4 actions that result in the excretion of more salt and water in the urine:

Dilate afferent arteriole and constricts efferent – increase GFR (more blood flow and higher GHP)

Antagonized angiotensin-aldosterone mechanism by inhibiting both renin and aldosterone secretion

Inhibits ADH

Inhibits NaCl reabsorption by the collecting ducts


A Summary of Renal Function

Figure 26.16b

Urinary system physiology

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