4.2: filtration & absorption

excretion of wastes

excretion separation & elimination of waste products

-nitrogenous wastes

stages of urine production

1. glomerular filtration

• majority of PLASMA pushed out of capillaries

2. tubular reabsorption

• necessary components returned to BLOOD

3. tubular secretion

• other substances selectively added

1. glomerular filtration

-water & solutes

-via

-water & solutes move from PLASMA into NEPHRON

-via hydrostatic pressure

filtration membrane (pt 1)

1. capillary wall

2. basement membrane

1. capillary wall

• fenestrated capillaries hold back blood cells & large proteins

2. basement membrane

• holds back most large molecules

filtration membrane (pt 2)

3. filtration slits

-spaces between

-most ___ molecules

-unless

3. filtration slits

• spaces between cells of visceral layer

• most small molecules can pass through (like water, electrolytes, glucose, wastes)

• unless bound to plasma proteins (like calcium, iron, thyroid hormone)

anything on left side would stay in circulatory system and not into urinary system

glomerular filtration pressure

-glomerular

→ driven

-outwards

-kidneys

-glomerular blood pressure is very high

→ driven by small diameter of EFFERENT arteriole

-outwards pressure always exceed inwards pressure → only filtration (FILTRATION = IN OR OUT OF TUBULE)

-kidneys very sensitive to hypertension

glomerular filtration rate (GFR)

-males: 125 mL/min or 180 L/day

-females: 105 mL/min or 150 L/day

-1-2L urine excreted daily

→ 99% of filtrate is reabsorbed

-amount of filtrate formed each minute by both kidneys

-GFR = NFP x Kf

→ NFP = net filtration pressure

the following makes up the filtration coefficient (Kf):

→ filtration membrane surface area

→ filtration membrane permeability

regulation of GFR

-GFR maintained by

-GFR maintained by adjusting glomerular blood pressure

-intrinsic controls: renal autoregulation

-extrinsic controls: nervous or hormonal regulation

intrinsic controls

-kidneys

→ activation

→ chemistry

-maintain

-kidneys regulate BP in response to internal stimuli:

→ activation of stretch receptors in afferent arteriole

→ chemistry of filtrate

-maintain dynamic equilibrium

extrinsic controls

-needed to

-neural control:

→ constricts

→ reduces

→ redirects

-needed to mediate larger changes in BP

-neural control: sympathetic stimulation

→ constricts afferent arteriole

→ reduces GFR & urine output

→ redirects blood away from kidneys

extrinsic control: renin-angiotensin-aldosterone (RAA) mechanism

ie

-decrease

-granular

→ sympathetic

→ signal

→ decreased

-renin

ie indirect renal mechanism

-decrease in systemic BP detected by baroreceptors, juxtagomerular apparatus

-granular cells release renin in response to:

→ sympathetic input

→ signal from macula densa (densely packed cells in kidney for sensory reception)

→ decreased stretch

-renin initiates production of angiotensin II

renin-angiotensin-aldosterone (RAA) mechanism

-vasoconstriction

→ raises

→ lowers

-stimulates

-acts

-overall

antiotensin II

-vasoconstriction of efferent arteriole

→ raises glomerular blood pressure → maintains GFR

→ lowers BP in peritubular capillaries/ vasa recta → enhances absorption (bc of decrease in hydrostatic BP and decreased resistance against vessel fluid movement)

-stimulates secretion of aldosterone and antidiuretic hormone → promote salt and water retension

-acts on hypothalamus to stimulate thirst

-overall effect is to increase systemic BP

tubular reabsorption

-primarily

-necessary

→ almost

→ H2O

-produces

-primarily takes place in PCT

-necessary water & solutes return to blood

→ almost all organic materials

→ H2O & some ions reabsorbed selectively

-produces hypertonic tubular fluid

reabsorption of sodium

-actively

→ symports:

-drives

-alters

-actively transported through TUBULE walls

→ symports: simulatneously binds Na+ and other solute

→ Na+ — H+ antiports

→ Na+ — K+ pumps

-drives reabsorption of everything else

-cotransportation

-alters osmotic & electrical gradients

reabsorption of water

-driven

-aquaporins:

→ always

→ inserted

-solvent drag:

-driven by osmotic gradient

-aquaporins: channels through tubule cells

→ always present in PCT → obligatory water reabsorption

→ inserted in collecting ducts only if ADH is present → facultative water reabsorption

-solvent drag: water carries along dissolved solutes

reabsorption of other solutes

-glucose, amino acids, vitamins, other ions

-nitrogenous wastes

-glucose, amino acids, vitamins, other ions

→ some co-transported with Na+

→ some carried with water

→ lipid-soluble solutes follow concentration gradient across tubule wall

-nitrogenous wastes

→ almost all uric acid

→ secreted back later

→ ~50% urea

→ but more diluted in blood than in urine

uptake by peritubular capillaries

capillary absorption driven by:

-accumulation of

-narrow

-plasma

-accumulation of reabsorbed fluid → high interstitial hydrostatic pressure (HPif)

-narrow efferent arterioles → low capillary hydrostatic pressure (HPc)

-plasma proteins retained during glomerular filtration: high colloid osmotic pressure (COPc)

(high HPif) + (high COPc) - (low HPc) = absorption

transport maximum (Tm)

-maximum amount of solute renal tubules can reabsorb (mg/ min)

-reached when transporters are saturated

→ sets maximum rate of reabsorption

-impacts reabsorption/ secretion of most solutes

→ each has its own Tm

glucosuria

-glucose in urine

-normally passes through renal tubule at 125mg/min

→ glucose Tm: 320mg/min

-high blood glucose increases glucose filtration (into tubule): may exeed Tm

-reduced H2O reabsorption

→ higher urine output

-associated with diabetes mellitus