Urine Formation And Micturition Phys

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electrolytes regulated by kidneys

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Sodium, chloride, potassium, calcium, phosphate,magnesium,

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Regulation of acid‐base balance:

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Hydrogen ions (pH)

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Excreted of metabolic waste products

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• Nitrogen (urea, ammonia, uric acid, creatinine)• Toxins, drugs, pesticides, food additives

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Secretion of hormones:

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• Renin ‐ controls the formation of angiotensin,

• Erythropoietin – stimulates red blood cell production,

• 1,25‐dihydroxyvitamin D – active form of vitamin D,influences calcium homeostasis

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Gluconeogenesis:

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Synthesis of glucose from amino acids

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Major cation and anion in extracellular fluids is

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Na+, Cl‐

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Major cation and anion in intracellular fluid is

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K+, PO43‐

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Two forces determine thismovement between compartments

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Hydrostatic and osmotic pressure

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Hydrostatic pressure (P)

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pressure forcing fluids across capillarywalls – generated by pumping of the heart

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Colloid Osmotic pressure (π)

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generated by osmotic proteins in fluidthat cannot cross the semi‐permeablemembrane

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Compartment 1 : compartment 2 Net Driving Pressure =

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(P1 – π1) – (P2 – π2)

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Changes in ECF volume & composition are mainlydetected through:

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-Low pressure baroreceptors (jugular, R atrium),

-Osmoreceptors (hypothalamus),

-Renal “baroreceptors”(gives rise to renin release & angiotensin formation),

-Adrenal cortex (zona glomerulosa cells, monitor K+),leading to aldosterone secretion

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renal corpuscle:

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(filtering component) consisting ofglomerulus and Bowman’s capsule

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Renal cortex:

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Site of glomerularfiltration & convolutedtubules

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Renal medulla:

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Location of longerloops of Henle &drainage of collectingducts into renal pelvis& ureter

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Urine formation

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Filtration,

Reabsorption,

Secretion,

Excretion.

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Glomerular filtration

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passive process,

Hydrostatic pressure forces fluids & solutesfrom glomerular capillaries into Bowman’sspace

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Tubular reabsorption

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Active & passive processes,

Movement of substances from the filtrate intubules into the peritubular capillaries,

Fluid taken back into body

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Tubular secretion

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Movement of substances from peritubularcapillaries to the tubules,

Remove fluid from body.

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Excretion

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Reabsorption of water through aldosterone mediated aquaporins,

Concentration of urine.

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3 layeredglomerular filtration barrier:

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– fenestrated (pores)endothelium of glomerularcapillaries,

– Basement membrane (-ve charge),

– Foot processes of podocytes &slit diaphragm.

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Course of Filtrate along tubule:

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cortex –medulla ‐ cortex – medulla – renal pelvis

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Filterability of solutes

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Size: (<7Da freely up to 70kDa),

Charge: (-ve charged molecules repelled by -ve charged membrane).

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pressure natriuresis

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Urine flow rate is proportional to arterialpressure

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2 mechanisms of Renal autoregulation

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1. Myogenic mechanism,

2. Tubuloglomerular feedback mechanism

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Myogenic mechanism:

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vascular smooth muscle Contracts when stretched (high bp) and Relaxes when not stretched (bp drop).

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Tubuloglomerular feedback mechanism:

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macular densa cells of thejuxtaglomerular complex: Senses Na+ content in distal tubule, (when Na+ low, increased Renin --> increased GFR).

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Biochemical tests of renal function:

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Urinalysis,

Measurement of GFR,

Tubular function tests

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Renal clearance (of a substance)

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Urine Flow Rate (ml/min) x [Urine] (mg/ml) / [Plasma] (mg/ml)

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Measurement of GFR

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Inulin:– Small, polysaccharide (5200 MW), => clearance of inulin = GRF

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Tubular secretion

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Eliminating undesirable substances or end productsthat have been reabsorbed by passive processes,

Eliminating excess K+ from the body,

regulating pH.

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Tubular reabsorption

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Highly selective: glucose, aminoacids, some ions;

process may be active orpassive:

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Active reabsorption:

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ATP required (directly: primary;indirectly secondary), pinocytosis(small proteins)

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Passive reabsorption:

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No ATP required. Diffusion,facilitated diffusion & osmosis downelectrochemical gradients

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Na+ reabsorption in proximal tubule

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1. Na+ diffuses across luminal (apical) membraneinto cell,

2. Primary active transport of Na+ by Na+/K+ATPase across basolateral membrane,

3. Passive absorption of Na+, waterfrom interstitial fluid into peritubular capillaryby ultrafiltration

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Glucose reabsorption (Secondary active transport)

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Sodium‐glucose co‐transporters (SGLT) on thebrush border of proximal tubular cells carryglucose into the cell, secondary active transport,against a concentration gradient.

Electrochemical gradient caused by Na+/K+ ATPase in the basolateralmembrane

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Proximal tubules

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High capacity for active & passive reabsorption– ~65% Na+, H20, 50% Cl‐, 90% HCO3‐, >90% K+– Most of glucose, lactose, amino acids

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Specialisations of proximal tubule epithelialcells

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large number of mitochondria (active transport),

– brush border (high surface area),

– Rapid transport of Na+ and other substances,

– Highly water permeable

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Transporters on the proximal tubule

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Lumenal: Na+/Gluc symporter, Na+/H+ antiporter,

Interstitial: Na+/K+ ATPase

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3 sections of Loop of Henle

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Thin descending segment, thin ascending segmentand thick ascending segment

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Thin descending limb:

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Highly permeable to water,10% reabsorbed– Water absorbed due to medullaryinterstitial Na+ concentration gradient.

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Thin Ascending limb

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– Virtually impermeable to water,

– low reabsorptive capacity

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Thick Ascending limb

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– Na+/K+ ATPases in the basolateralmembranes– Low intracellular Na+ provides gradientfor driving a protein carrier that alsodrives the reabsorption of K + and Cl‐:the 1 Na+ , 2Cl‐, 1K+ cotransporter

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Early distal tubule

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First section forms the macula densa – partof the juxtaglomerular apparatus

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Late distal tubule

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aldosterone-dependant Na+ resorption,

Na+/K+ ATPases– Reabsorbed with Cl‐ symporter.

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Collecting Duct

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ADH /vasopressin– Dependent:

aquaporins are mobilised tomembrane of cells and facilitate movement ofwater out of tubules by osmosis

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Two cell types of late distal tubule &collecting duct

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1. Principal cells

2. Intercalated cells

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Principal cells

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reabsorb Na+ & secrete K+,

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Intercalated cells

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secrete H+ & reabsorb HCO3‐ & K+(important for acid‐base balance)

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Four areas where ECF is monitored

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Hypothalamus,

Adrenal cortex,

Peripheral Baroreceptors,

Renal baroreceptors.

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Hypothalamus: Osmoreceptors

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increased osmolarity →osmoreceptor cells in theanterior hypothalamus toshrink → Shrinkage of cells causes actionpotentials → posteriorpituitary → ADH released → water resorption.

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Adrenal cortex: zonaglomerulosa

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↑plasma K+ or angiotensin II → Aldosterone released → reabsorptionof Na+

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Peripheral Baroreceptors:

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aortic and carotid sinuses:

↑ in volume →Na + excretion,

↓ in volume → inhibits Na + excretion (=> ↑ECFvolume)

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Renal Baroreceptors: Control renin release

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Granular cells, Sympathetic nerves and Macula Densa

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Granular cells in arteriolar walls sensepressure

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↑BP → ↓renin release;

↓ BP → ↑ renin release => increase salt &water reabsorption by kidney

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Sympathetic nerves

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Increased activity causes renin release & viceversa

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Macula densa cells: Chemoreceptors

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Drop in flow rate leads to increased reabsorptionof NaCl in ascending loop of Henle, reducingconcentration of NaCl at macula densa →increases renin release

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Extrinsic Mechanisms of renal output

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1. Sympathetic nerves (short term)• Arterioles, proximal tubule, granular cells,

2. Hormones (medium ‐ long term)• AngII, aldosterone, ADH, atrial natriuretic peptide (ANP)

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Intrinsic Mechanisms of renal output

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1. Pressure natriuresis/diuresis, autoregulation• Myogenic mechanism, tubulo‐glomerular feedback (TGF),

2. Local factors• Nitric oxide (vasodilator), prostaglandins (vasodilators),endothelin (vasoconstrictor)

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Produced by adrenal cortex & stimulates sodiumreabsorption in the collecting ducts,

Increases Na+/K+ ATPases inbasolateral membrane of epithelial cells of collectingduct,

sodium reabsorption

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Aldosterone

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Activation results inincreased waterreabsorption by insertion ofaquaporins into luminalsurface of tubular epithelialcells

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Anti‐diuretic hormone

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Activation results in decreased water and sodiumreabsorption (i.e. Increased water & sodiumexcretion),

inhibits secretion of renin and aldosterone

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Atrial natriuretic peptide (ANP)

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Effect of Dehydration

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cells shrink signalling to posteriorpituitary to release ADH → insertion of ready made aquaporinsinto luminal membrane of collecting duct →↑water reabsorption.

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Effect of Haemorrhage

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drop in arterial pressure → reduces GFR → ↑ Na reabsorption → Increased renin release → ↑ AngII → ↑aldosterone → ↑ Na and water retention.

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Effect of Congestive heart failure

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Reduced CO → reduced atrial pressure → reduced GFR → ↑ [Na+] → ↑ renin release → ↑ AngII → ↑aldosterone → ↑ Na and water retention.

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3 layers of the bladder

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1. outer serosal layer,

2. thick muscular (smooth muscle)layer,

3. Internal transitionalepithelium.

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Bladder filling

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Sympathetic NS relaxes bladder &contracts internal sphincter &inhibits PSNS ganglionic transmission,

somatic motor neurons contractexternal sphincter

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Bladder emptying

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micturition centre in braininhibit SNS nerves & therefore removesSNS inhibition of PSN ganglionic transmission,

internal sphincter relaxes, bladder contracts,

somatic motor neurons inhibited to relaxexternal sphincter.

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damage to sensory nerve fibres,

Micturition reflex impaired,

Bladder fills to capacity and overflows a few drops at a time.

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Overflow incontinence

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involuntary loss of urine arising from increasedintra‐abdominal pressure e.g. coughing, sneezing,bending down, lifting

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Stress incontinence

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Result of lesions between the pontine storage & micturition centresand the lower spinal cord,

No voluntary control over external urethral sphincter, involuntary voiding,

Bladder never emptied completely

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Automatic bladder