Urinary System (Anatomy and Physiology)

THE URINARY SYSTEM PART I OBJECTIVES: The student should be able to: 1. List several kidney functions that help maintain body homeostasis. 2. Describe, in order, the components of a nephron, state the function of each component, and label each in a rough sketch of a nephron. 3. List the components of the filtration membrane. List and describe the forces acting at the filtration membrane and, given values for each, calculate the net filtration pressure (NFP). 4. Contrast the purposes of intrinsic and extrinsic control of glomerular filtration rate (GFR). Include a detailed discussion of renal autoregulation and neural and hormonal control. (See Figure 25.14.) 5. Describe in detail the active and passive mechanisms involved in the tubular reabsorption of sodium, glucose, amino acids, Cl-, H2O, and urea. State how and in which part of the nephron sodium reabsorption is controlled and the reasons why control of sodium reabsorption is critical. 6. Describe the role of tubular secretion in altering the composition of tubular fluid. OBJECTIVES: The student should be able to: 7. Explain the role of aldosterone and of atrial natriuretic peptide (ANP) in sodium and water balance. 8. Describe how the renal medullary osmotic gradient is created and maintained (see Focus Figure 25.1 on pp. 982-983). 9. Sketch a juxtamedullary nephron within the kidney, clearly showing the location of the ascending and descending limbs of the nephron loop and a collecting duct. Give values for the osmolality of the interstitial fluid in the cortex and the various parts of the medulla in your diagram, and for the osmolalities of fluids in the two limbs of the nephron loop and in the distal tubule. 10. Explain the mechanisms that allow for the formation of dilute or concentrated urine. On a diagram, show the osmolality in the collecting duct in the presence or absence of ADH. (Fig. 25.19) 11. Describe the normal physical and chemical properties of urine. 12. Define micturition and describe its neural control. Key Terms: Excretion nephron, glomerulus, renal tubule, glomerular capsule, renal corpuscle, filtrate, podocytes, foot processes, filtration slits, capsular space, proximal convoluted tubule (PCT), nephron loop (loop of Henle), descending limb, ascending limb, distal convoluted tubule (DCT), collecting duct, cortical nephrons, juxtamedullary nephrons, afferent arteriole, efferent arteriole, peritubular capillaries, vasa recta, juxtaglomerular complex (JGC), granular (juxtaglomerular) cells, macula densa, filtration membrane glomerular filtration, net filtration pressure (NFP), glomerular hydrostatic pressure (HPgc), colloid osmotic pressure in glomerular capillaries (OPgc), hydrostatic pressure in the capsular space (HPcs), glomerular filtration rate (GFR), renal autoregulation, myogenic mechanism, tubuloglomerular feedback mechanism tubular reabsorption, apical membrane, basolateral membrane, sodium reabsorption, aquaporins, obligatory water reabsorption, transport maximum (Tm), urea, creatinine, uric acid, atrial natriuretic peptide (ANP) Key Terms: tubular secretion osmolality, countercurrent mechanism, countercurrent multiplier, countercurrent exchanger, medullary osmotic gradient, antidiuretic hormone (ADH, vasopressin), facultative water reabsorption, diuretics renal clearance ureters, urinary bladder, detrusor, urethra, internal urethral sphincter, external urethral sphincter, micturition (voiding, urination), pontine micturition center Function of Kidneys Regulate total water volume and total solute concentration in water Regulate ion concentrations in extracellular fluid (ECF) Ensure long-term acid-base balance Excrete metabolic wastes, toxins, drugs Endocrine functions: Produce erythropoietin (regulates RBC production) Produce renin (regulates blood pressure) Activate vitamin D Carry out gluconeogenesis, if needed Figure 25.1 The urinary system. Anatomy of Kidneys Gross and internal anatomy - self study Figure 25.4 Internal anatomy of the kidney. Blood and Nerve Supply Blood: kidneys cleanse blood and adjust its composition, so it has a rich blood supply Renal arteries deliver about one-fourth (1200 ml) of cardiac output to kidneys each minute Nerve supply: via sympathetic fibers from renal plexus Figure 25.5a Blood vessels of the kidney. Figure 25.5b Blood vessels of the kidney. Nephrons the structural and functional units that form urine > 1 million per kidney Two main parts: Renal corpuscle Glomerulus Glomerular capsule (Bowman’s capsule) Renal tubule Figure 25.6 Location and structure of nephrons. Figure 25.7 Renal cortical tissue. Renal Corpuscle Two parts: 1. Glomerulus Tuft of capillaries composed of fenestrated endothelium Highly porous capillaries, allows for efficient filtrate formation Filtrate: plasma-derived fluid that renal tubules process to form urine 2. Glomerular capsule cup-shaped, hollow structure surrounding glomerulus Consists of two layers: Parietal layer : simple squamous epithelium Visceral layer : clings to glomerular capillaries; branching epithelial podocytes Extensions terminate in foot processes that cling to basement membrane Filtration slits between foot processes allow filtrate to pass into capsular space Figure 25.6-2 Location and structure of nephrons. Renal Tubule Consists of single layer of epithelial cells, but each region has its own unique histology and function Three major parts: 1. Proximal convoluted tubule Proximal, closest to renal corpuscle 2. Nephron loop 3. Distal convoluted tubule Distal, farthest from renal corpuscle Distal convoluted tubule drains into collecting duct Figure 25.6-4 Location and structure of nephrons. 2. Nephron loop U-shaped structure consisting of two limbs Descending limb Proximal part of descending limb is continuous with proximal tubule Distal portion also called descending thin limb; simple squamous epithelium Ascending limb Thick ascending limb Thin in some nephrons Cuboidal or columnar cells 3. Distal convoluted tubule (DCT) Cuboidal cells with very few microvilli Function more in secretion than reabsorption Confined to cortex Collecting ducts Two cell types: Principal cells Sparse with short microvilli Maintain water and Na+ balance Intercalated cells Cuboidal cells with abundant microvilli Two types of intercalated cells A and B: both help maintain acid-base balance of blood receive filtrate from many nephrons Run through medullary pyramids Give pyramids their striped appearance Ducts fuse together to deliver urine through papillae into minor calyces Figure 25.6-7 Location and structure of nephrons. Figure 25.6 Location and structure of nephrons. Classes of Nephrons 1. Cortical nephrons Make up 85% of nephrons Almost entirely in cortex 1. Juxtamedullary nephrons Long nephron loops deeply invade medulla Ascending limbs have thick and thin segments Important in production of concentrated urine*** Figure 25.8 Cortical and juxtamedullary nephrons, and their blood vessels. Nephron Capillary Beds Renal tubules are associated with two capillary beds: Glomerulus Peritubular capillaries Juxtamedullary nephrons are associated with Vasa recta Nephron Capillary Beds (cont.) Glomerulus Capillaries are specialized for filtration Different from other capillary beds because they are fed and drained by arteriole Afferent arteriole enters glomerulus and leaves via efferent arteriole Efferent feed into either peritubular capillaries or vasa recta Blood pressure in glomerulus high because: Afferent arterioles are larger in diameter than efferent arterioles Arterioles are high-resistance vessels Peritubular capillaries Low-pressure, porous capillaries adapted for absorption of water and solutes Arise from efferent arterioles Cling to adjacent renal tubules in cortex Empty into venules Vasa recta Long, thin-walled vessels parallel to long nephron loops of juxtamedullary nephrons Arise from efferent arterioles serving juxtamedullary nephrons Instead of peritubular capillaries Function in formation of concentrated urine Figure 25.9 Blood vessels of the renal cortex. Figure 25.8 Cortical and juxtamedullary nephrons, and their blood vessels. Juxtaglomerular Complex (JGC) Each nephron has one juxtaglomerular complex (JGC) Involves modified portions of: Distal portion of ascending limb of nephron loop Afferent (sometimes efferent) arteriole Important in regulating rate of filtrate formation and blood pressure Three cell populations: Macula densa cells, granular cells, extraglomerular mesangial cells Juxtaglomerular Complex (JGC) (cont.) Macula densa cells Tall, closely packed cells of ascending limb Contain chemoreceptors that sense NaCl content of filtrate Granular cells (juxtaglomerular, or JG cells) Enlarged, smooth muscle cells of arteriole Act as mechanoreceptors to sense blood pressure in afferent arteriole secretory granules contain enzyme renin Figure 25.10 Juxtaglomerular complex (JGC) of a nephron. CHAPTER 25 THE URINARY SYSTEM PART II Kidney Physiology: Urine formation 180 L of fluid processed daily; only 1.5 L of urine is formed Consume 20–25% of oxygen used by body at rest Filtrate (produced by glomerular filtration) is basically blood plasma minus proteins Urine is produced from filtrate Urine <1% of original filtrate Contains metabolic wastes and unneeded substances Three processes are involved in urine formation and adjustment of blood composition: 1. Glomerular filtration: produces cell- and protein-free filtrate 2. Tubular reabsorption: selectively returns 99% of substances from filtrate to blood in renal tubules and collecting ducts 3. Tubular secretion: selectively moves substances from blood to filtrate in renal tubules and collecting ducts Figure 25.11 The three major renal processes. Glomerular Filtration a passive process No metabolic energy required Hydrostatic pressure forces fluids and solutes through filtration membrane into glomerular capsule No reabsorption into capillaries of glomerulus The Filtration Membrane Porous membrane between blood and interior of glomerular capsule Allows water and solutes smaller than plasma proteins to pass Normally no cells can pass Allows molecules smaller than 3 nm to pass Water, glucose, amino acids, nitrogenous wastes Does not allow cells or plasma proteins Plasma proteins remain in blood to maintain colloid osmotic pressure  Prevents loss of all water to capsular space The Filtration Membrane (cont.) Contains three layers: 1. Fenestrated endothelium of glomerular capillaries 2. Basement membrane: fused basal laminae of two other layers 3. Foot processes of podocytes with filtration slits; slit diaphragms repel macromolecules Figure 25.12a The filtration membrane. Figure 25.12b The filtration membrane. Figure 25.12c The filtration membrane. Figure 25.12d The filtration membrane. Pressures That Affect Filtration Outward pressures Forces that promote filtrate formation Hydrostatic pressure in glomerular capillaries (HPgc) = glomerular blood pressure Chief force pushing water, solutes out of blood Quite high: 55 mm Hg*** Compared to ~ 26 mm Hg seen in most capillary beds Reason: efferent arteriole is a high-resistance vessel with a diameter smaller than afferent arteriole Pressures That Affect Filtration (cont.) Inward Pressures Forces inhibiting filtrate formation: Hydrostatic pressure in capsular space (HPcs): filtrate pressure in capsule; 15 mm Hg Colloid osmotic pressure in capillaries (OPgc): “pull” of proteins in blood; 30 mm Hg Net filtration pressure (NFP): sum of forces Outward - inward Pressure responsible for filtrate formation Figure 25.13 Forces determining net filtration pressure (NFP). volume of filtrate formed per minute by both kidneys (normal = 120–125 ml/min) GFR is directly proportional to: Net filtration pressure (NFP) Total surface area available for filtration Filtration membrane permeability Much more permeable than other capillaries Controlled via glomerular hydrostatic pressure If rises  NFP rises  GFR rises (urine output  BP) If falls only 18% GFR = 0 Regulation of Glomerular Filtration 1. Intrinsic controls: renal autoregulation renal autoregulation to maintain GFR when MAP in range of 80–180 mm Hg Two types of renal autoregulation: a) Myogenic mechanism b) Tubuloglomerular feedback mechanism 1. Extrinsic controls Neural and hormonal controls systemic BP < 80 or > 180 mm Hg Intrinsic controls: Renal autoregulation Maintains nearly constant GFR when MAP is in range of 80–180 mm Hg Autoregulation ceases if out of that range Two types of renal autoregulation: 1. Myogenic mechanism 2. Tubuloglomerular feedback mechanism Intrinsic controls (cont’d) 1. Myogenic mechanism Local smooth muscle contracts when stretched Increased BP causes muscle to stretch, leading to constriction of afferent arterioles Restricts blood flow into glomerulus Protects glomeruli from damaging high BP Decreased BP causes dilation of afferent arterioles Both help maintain normal GFR despite normal fluctuations in blood pressure Intrinsic controls (cont’d) 2. Tubuloglomerular feedback mechanism Flow-dependent mechanism directed by macula densa cells Respond to filtrate’s NaCl concentration If GFR increases, filtrate flow rate increases Leads to decreased reabsorption time, causing high NaCl levels in filtrate Feedback mechanism causes constriction of afferent arteriole, which lowers NFP and GFR, allowing more time for NaCl reabsorption Opposite mechanism for decreased GFR Extrinsic controls: Neural and hormonal mechanisms Purpose of extrinsic controls is to regulate GFR to maintain systemic blood pressure Extrinsic controls will override renal intrinsic controls if blood volume needs to be increased Neural: sympathetic NS Hormonal: renin-angiotensin-aldosterone mechanism Sympathetic nervous system Under normal conditions at rest Renal blood vessels dilated Renal autoregulation mechanisms prevail Under abnormal conditions, such as extremely low ECF volume (low blood pressure) Norepinephrine is released by sympathetic nervous system and epinephrine is released by adrenal medulla, causing: Systemic vasoconstriction, which increases blood pressure Constriction of afferent arterioles, which decreases GFR Blood volume and pressure increases Extrinsic controls (cont’d) Renin-angiotensin-aldosterone mechanism Main mechanism for increasing blood pressure Three pathways to renin release by granular cells 1. Direct stimulation of granular cells by sympathetic nervous system 2. Stimulation by activated macula densa cells when filtrate NaCl concentration is low 3. Reduced stretch of granular cells Figure 25.14 Regulation of glomerular filtration rate (GFR) in the kidneys. • • • • • Tubular Reabsorption most of tubular contents reabsorbed and returns to blood Selective transepithelial process – All organic nutrients are reabsorbed – Water and ion reabsorption is hormonally regulated and adjusted Includes active and passive tubular reabsorption Substances can follow two routes: – Transcellular – Paracellular – Tubular Reabsorption – Transcellular route • Solute enters apical membrane of tubule cells • Travels through cytosol of tubule cells • Exits basolateral membrane of tubule cells • Enters blood through endothelium of peritubular capillaries – Paracellular route • Between tubule cells – Limited by tight junctions, but leaky in proximal nephron Water, Ca2+, Mg2+, K+, and some Na+ in the PCT move via this route – Figure 25.15 Transcellular and paracellular routes of tubular reabsorption. Tubular Reabsorption of Sodium Na+ - most abundant cation in filtrate – Most is reabsorbed before the filtrate reaches the DCT Sodium transport across the basolateral membrane: – via primary active transport – Na+-K+ ATPase pumps Na+ into interstitial space  low intracellular Na+ levels – Na+ is then swept by bulk flow into peritubular capillaries Sodium transport across apical membrane: – via secondary active transport (cotransport) or via facilitated diffusion through channels • Active pumping of Na+ at basolateral membrane  low intracellular Na+ levels  facilitates Na+ diffusion across apical membrane – Tubular Reabsorption of Nutrients, Water, and Ions Na+ reabsorption by primary active transport drives reabsorption of most other substances – Organic nutrients reabsorbed by secondary active transport are cotransported with Na+ at luminal membrane • Glucose, amino acids, some ions (e.g. Bicarbonate), vitamins – Tubular Reabsorption of Nutrients, Water, and Ions (cont.) Passive tubular reabsorption of water – Movement of Na+ and other solutes creates osmotic gradient for water – Water is reabsorbed by osmosis, aided by water-filled pores called aquaporins • Obligatory water reabsorption – Aquaporins are always present in PCT • Facultative water reabsorption – Aquaporins are inserted in collecting ducts only if ADH is present Tubular Reabsorption of Nutrients, Water, and Ions (cont.) Passive tubular reabsorption of solutes – Solute concentration in filtrate increases as water is reabsorbed • Creates concentration gradients for solutes, which drive their entry into tubule cell and peritubular capillaries – Fat-soluble substances, some ions, and urea will follow water into peritubular capillaries down their concentration gradients • lipid-soluble drugs and environmental pollutants are reabsorbed even though it is not desirable Figure 25.16 Reabsorption by PCT cells. Transport Maximum Transcellular transport systems are specific and limited » • • • • • • • • • • • Transport maximum (Tm) exists for almost every reabsorbed substance • Reflects number of carriers in renal tubules that are available – When carriers for a solute are saturated, Tm is exceeded and excess of solute is excreted in urine Reabsorptive Capabilities of Renal Tubules and Collecting Ducts Proximal convoluted tubule – Site of most reabsorption • All nutrients, such as glucose and amino acids, are reabsorbed • 65% of Na+ and water reabsorbed • Many ions • Almost all uric acid • About half of urea (later secreted back into filtrate) Reabsorptive Capabilities of Renal Tubules and Collecting Ducts (cont.) Nephron loop – Descending limb: H2O can leave, solutes cannot – Ascending limb: H2O cannot leave, solutes can • Thin segment is passive to Na+ movement • Thick segment has Na+-K+-2Cl– symporters and Na+-H+ antiporters that transport Na+ into cell – Some Na+ can pass into cell by paracellular route in this area of limb Reabsorptive Capabilities of Renal Tubules and Collecting Ducts (cont.) Distal convoluted tubule and collecting duct – Reabsorption is hormonally regulated in these areas – Antidiuretic hormone (ADH) • Released by posterior pituitary gland • Causes principal cells of collecting ducts to insert aquaporins in apical membranes, increasing water reabsorption – Increased ADH levels cause an increase in water reabsorption Reabsorptive Capabilities of Renal Tubules and Collecting Ducts (cont.) – Aldosterone • Targets collecting ducts (principal cells) and distal DCT • Promotes synthesis of apical Na+ and K+ channels, and basolateral Na+-K+ ATPases for Na+ reabsorption (water follows) • Without aldosterone, daily loss of filtered Na+ would be 2%, which is incompatible with life • Functions: increase blood pressure and decrease K+ levels Reabsorptive Capabilities of Renal Tubules and Collecting Ducts (cont.) – Atrial natriuretic peptide • Reduces blood Na+, resulting in decreased blood volume and blood pressure – • • • • • • • • Released by cardiac atrial cells if blood volume or pressure elevated • Opposite to aldosterone – Parathyroid hormone • Acts on DCT to increase Ca2+ reabsorption Figure 25.17 Summary of tubular reabsorption and secretion. Table 25.1-1 Reabsorption Capabilities of Different Segments of the Renal Tubules and Collecting Ducts Table 25.1-2 Reabsorption Capabilities of Different Segments of the Renal Tubules and Collecting Ducts (continued) Table 25.1-3 Reabsorption Capabilities of Different Segments of the Renal Tubules and Collecting Ducts (continued) Tubular Secretion is reabsorption in reverse Occurs almost completely in PCT Selected substances are moved from peritubular capillaries through tubule cells out into filtrate – K+, H+, NH4+, creatinine, organic acids and bases – Substances synthesized in tubule cells also are secreted (example: HCO3–) Tubular Secretion is important for: – Disposing drugs or metabolites bound to plasma proteins – Eliminating undesirable substances that were passively reabsorbed (example: urea and uric acid) – Ridding body of excess K+ (aldosterone effect) – Controlling blood pH by altering amounts of H+ or HCO3– in urine Figure 25.17 Summary of tubular secretion. Regulation of Urine Concentration and Volume Osmolality – Number of solute particles in 1 kg of H2O – Reflects ability to cause osmosis Osmolality of body fluids – Expressed in milliosmols (mOsm) – Kidneys maintain osmolality of plasma at ~300 mOsm by regulating urine concentration and volume – Kidneys regulate with countercurrent mechanism Countercurrent Mechanism Occurs when fluid flows in opposite directions in two adjacent segments of same tube with hair pin turn Two parts: – Countercurrent multiplier – interaction of filtrate flow in ascending/descending limbs of nephron loops of juxtamedullary nephrons • • • • • • • • • • • • • • • • • • Countercurrent exchanger - Blood flow in ascending/descending limbs of vasa recta – The countercurrent mechanisms work together to: • Establish and maintain medullary osmotic gradient from renal cortex through medulla – Gradient runs from 300 mOsm in cortex to 1200 mOsm at bottom of medulla – Countercurrent multiplier creates gradient – Countercurrent exchanger preserves gradient • Collecting ducts can then use gradient to vary urine concentration Focus Figure 25.1a Juxtamedullary nephrons create an osmotic gradient within the renal medulla that allows the kidney to produce urine of varying concentration. Countercurrent Multiplier: Nephron Loop SETS osmotic gradient depends on: – Difference in permeabilities between descending nephron loop and ascending loop Descending limb – freely permeable to H2O, impermeable to solutes – H2O passes out of filtrate into hyperosmotic medullary interstitial fluid • Causes remaining filtrate osmolality to increase to ~1200 mOsm Ascending limb – impermeable to H2O, selectively permeable to solutes • Na+ and Cl– are actively reabsorbed in thick segment (some passively reabsorbed in thin segment) • Filtrate osmolality decreases to 100 mOsm – Focus Figure 25.1b Juxtamedullary nephrons create an osmotic gradient within the renal medulla that allows the kidney to produce urine of varying concentration. Countercurrent Exchanger: Vasa recta Maintains medullary gradient highly permeable to water and solutes – blood can exchange NaCl and water with surrounding interstitial fluid as it moves through adjacent parallel sections of gradient • Blood inside vasa recta remains isosmotic with surrounding interstitial fluid Figure 25.18 Countercurrent exchange. Formation of Dilute or Concentrated Urine Established medullary osmotic gradient can be used to form urine > 300 mOsm to conserve water Overhydration produces large vol. of dilute urine – ADH production decreases; urine ~100 mOsm – If aldosterone present, additional ions can be removed, causing water to dilute to ~50 mOsm – • • • • • • • • • • • • • • • • • • • • • • • • • Dehydration produces small vol. of concentrated urine – Maximal ADH is released; urine ~1200 mOsm – Severe dehydration: 99% water reabsorbed – Figure 25.19a Mechanism for forming dilute or concentrated urine. Figure 25.19b Mechanism for forming dilute or concentrated urine. Urea Recycling and the Medullary Osmotic Gradient Urea helps form medullary gradient – Urea enters filtrate in ascending thin limb of nephron loop by facilitated diffusion – Cortical collecting duct reabsorbs water, leaving urea behind – In deep medullary region, now highly concentrated urea leaves collecting duct and enters interstitial fluid of medulla • Urea then moves back into ascending thin limb • Contributes to high osmolality in medulla Diuretics Chemicals that enhance urinary output – ADH inhibitors, such as alcohol – Substances that inhibit Na+ reabsorption (and resultant H2O reabsorption) • e.g. caffeine or drugs for hypertension or edema – Osmotic diuretics: substance not reabsorbed, so water remains in urine; • e.g. in diabetic patient, high glucose concentration pulls water from body Renal Clearance volume of plasma kidneys can clear of a particular substance in a given time (ml/min) Renal clearance tests are used to determine GFR & status of kidney function – To help detect glomerular damage – To follow progress of renal disease Renal clearance rate is calculated as: C = UV/P – C = renal clearance rate (ml/min) – U = concentration (mg/ml) of substance in urine – V = flow rate of urine formation (ml/min) – P = concentration of same substance in plasma – Physical Characteristics of Urine Color and transparency – Clear • Cloudy may indicate urinary tract infection – Pale to deep yellow from urochrome • Pigment from hemoglobin breakdown • Yellow color deepens with increased concentration – Abnormal color (pink, brown, smoky) • Can be caused by certain foods, bile pigments, blood, drugs Odor – Slightly aromatic when fresh – Develops ammonia odor upon standing – May be altered by some drugs, vegetables or disease • Patients with diabetes may have acetone smell to urine – Physical Characteristics of Urine • • • • • • • • • • • • • • • • • pH – Urine is slightly acidic (~pH 6, with range of 4.5 to 8.0) – Acidic diet (protein, whole wheat) can cause drop in pH – Alkaline diet (vegetarian), prolonged vomiting, or urinary tract infections can cause an increase in pH Specific gravity – Ranges from 1.001 to 1.035 depending on solute concentration – specific gravity of water = 1 Chemical composition of Urine 95% water and 5% solutes Nitrogenous wastes – Urea (from amino acid breakdown): largest solute component – Uric acid (from nucleic acid metabolism) – Creatinine (metabolite of creatine phosphate) Other normal solutes found in urine – Na+, K+, PO43–, and SO42–, Ca2+, Mg2+ and HCO3– Presence of blood proteins, blood cells and bile pigments may indicate pathology – Table 25.2 Abnormal Urinary Constituents Transport, Storage, and Elimination of Urine Ureters slender tubes that convey urine from kidneys to bladder – Begin at L2 as continuation of renal pelvis Retroperitoneal Enter base of bladder through posterior wall – As bladder pressure increases, distal ends of ureters close, preventing backflow of urine • Urinary Bladder Muscular sac for temporary storage of urine Retroperitoneal, on pelvic floor posterior to pubic symphysis – Males: prostate inferior to bladder neck – Females: anterior to vagina and uterus Has openings for ureters and urethra – Trigone • Smooth triangular area outlined by openings for ureters and urethra • Infections tend to persist in this region Collapses when empty; Rugae appear Expands and rises superiorly during filling without significant rise in internal pressure • • • • • • • • • • • • • • • • Figure 25.21b Structure of the urinary bladder and urethra. Urethra Muscular tube that drains urinary bladder Sphincters – closed except when urine is being passed – Internal urethral sphincter • Involuntary (smooth muscle) at bladder-urethra junction • Contracts to open – External urethral sphincter • Voluntary (skeletal) muscle surrounding urethra as it passes through pelvic floor Urethra (cont.) Female urethra: – tightly bound to anterior vaginal wall – Shorter than male’s • External urethral orifice: anterior to vaginal opening; posterior to clitoris Male urethra carries semen and urine – Three named regions Figure 25.21a Structure of the urinary bladder and urethra. Micturition also called urination or voiding Three simultaneous events must occur – Contraction of detrusor by ANS – Opening of internal urethral sphincter by ANS – Opening of external urethral sphincter by somatic nervous system Micturition (cont.) Reflexive urination (urination in infants) – Distension of bladder activates stretch receptors – Causes excitation of parasympathetic neurons in reflex center in sacral region of spinal cord to cause: • contraction of detrusor • opening (contraction) of internal sphincter – Inhibition of somatic pathways to external sphincter, allowing its relaxation (opening) for urine flow Micturition (cont.) Pontine control centers mature between ages 2 and 3; override reflexive urination – Pontine storage center inhibits micturition • Inhibits parasympathetic pathways • Excites sympathetic and somatic efferent pathways – Pontine micturition center promotes micturition • Excites parasympathetic pathways • Inhibits sympathetic and somatic efferent pathways Figure 25.23 Control of micturition. • Test your knowledge: Do the following Review Questions at the end of Chapter 25: 1-7 and 10-22