Questions

• Path of blood from renal artery to afferent arteriole


  Renal a interlobar arcuate cortical radiate/interlobular afferent a
• Pathway for filtered fluid (filtrate) from glomerulus to collecting duct


  Glomerulus Bowman's capsule proximal CT thin descending loop thick ascending loop distal CT collecting duct
• Fenestrae


  Windows that help selectively filter blood through the glomerulus
• Differences between cortical and juxtamedullary nephrons

  • Cortical – shorter loops, receive blood from peritubular capillaries
  • Juxtamedullary – long loops, blood from vasa recta (more concentrating effect = countercurrent)
• Juxtaglomerular apparatus (JGA)


  • Macula densa (special cells of DCT) meet juxtaglomerular cells (smooth muscle cells of afferent arteriole)
  • Regulate blood pressure (renin) and glomerular filtration rate (TG feedback)
• Principal cells of DCT

  Respond to aldosterone
• Mechanism of glomerular filtration


  1. Filtration – forces exerted to move fluid/small molecules out of glomerulus into Bowman's capsule prior to rest of nephron influence

  2. GCP – glomerular capillary pressure, out of capillary into Bowman's

  3. CHP – capsular hydrostatic pressure, against GCP

  4. BCOP – blood colloid osmotic pressure, blood protein attraction of H2O, against GCP
• Intrinsic control (autoregulation) of GFR


  1. Myogenic – afferent arteriole vasoconstriction in response to high systemic BP to decrease renal blood flow (opposite too – vasodilation in response to low systemic BP)

  2. TG feedback – macula densa detects filtrate/urine flow to signal JG cells to change afferent arteriole diameter (ie. decreased filtrate/urine flow a.a. vasodilation increase blood flow increase filtrate/urine flow)
• Renin-angiotensin-aldosterone extrinsic control mechanism

  1. Renin from JG cells of JGA in response to low BP/low filtrate/urine delivery converts angiotensinogen (liver) to angiotensin I ACE (lungs/kidneys) converts AI to AII

  2. AII – vasoconstrictor, + aldosterone release (^ Na and H2O reabsorption at DCT), + thirst ^ BV ^BP
• Autonomic nervous system regulation of GFR extrinsically


  Sympathetic + afferent arteriole vasoconstriction decreases BP and GFR to glomerulus and redirects blood to other body tissues (ie. skeletal muscle)
• Glucose or glycine (amino acid) reabsorption through the PCT


  1. Na/K/ATPase primary active transport pump in basolateral membrane makes Na low inside PCT cell

  2. Na has concentration gradient from high (filtrate/urine) into cell (low) and diffuses into cell

  3. Glucose or amino acids "hitch a ride" with Na via symport = secondary active transport

  4. Glucose or amino acids concentrate inside PCT cell so transported via facilitated diffusion from PCT cell to blood
• Transport maximum


  • Too much filtered blood glucose will exceed transport/reabsorption of glucose carriers in the PCT
  • Glucose will stay in urine and cause osmotic attraction of H2O dehydration
• Differences between thin and thick limbs of the nephron loop


  • Thin – most H2O reabsorption due to surrounding interstitial, as descend increasing solute (urea) concentration driving osmosis maximal concentration of 1200 mOsm
  • Thick – most solute transport via Na/K/2Cl symport using secondary active transport, as ascend tubular fluid more dilute due to reabsorbed solutes (but volume low as much H2O already absorbed due to thin descending)
  • Due to surrounding vasa recta removal of solutes and water, interstitial concentrations remain intact and drive the countercurrent mechanism
• Aldosterone action on the DCT


  Stimulates synthesis/insertion of transport channels and pumps to increase Na and H2O reabsorption (and K secretion) in the principal cells of DCT
• ADH action on the collecting duct


  • Inserts aquaporin water channels into principal cells of collecting duct
  • Using increasing interstitial concentration as move down the CD, more and more H2O is removed from filtrate/urine via osmosis
• Diabetes insipidus


  Insufficient ADH secretion or response to ADH could create fatal dehydration
• Direction of solute secretion


  • Secretion of solutes - transport from nearby blood to interstitium to inside the tubule (the reverse of reabsorption direction)
  • K and H at DCT
  • H at PCT
• Carbonic anhydrase action in PCT cell

  1. CO2 (from lumen/filtrate/lumen) + H2O H2CO3 (by CA) HCO3- (to blood) + H+ (to filtrate/urine)

  2. H+ secretion is secondary active transport (uses Na/H antiporter and Na concentration gradient "energy")
• Micturition in infants and adults


  1. Infants - stretch receptors in bladder wall sense increase in volume reflex activation of parasympathetic output to contract bladder detrusor and relax IUS, also decreases somatic path signal to EUS to cause relaxation (not well developed in infants anyway)

  2. Adults – cerebral/pons descending spinal path develops to regulate parasympathetic and somatic paths to bladder and EUS voluntarily
• Duct pathway for spermatozoa from formation in the testes to release


  Seminiferous tubules rete testesepididymisductus deferensurethra
• Locations and functions of Sertoli and Leydig cells


  • Sertoli – inside seminiferous tubules; support, protect, nourish, stimulate release of sperm, form blood/testes barrier
  • Leydig – just outside seminiferous tubules (still in testes); secrete testosterone
• Meiosis in spermatogenesis


  1. Stem cell spermatogonia are 2N (46) and remains 2N as primary spermatocyte

  2. Primary spermatocytes undergo Meiosis I to make secondary spermatocytes so then have 1N (23) but double chromatids (arms)

  3. Meiosis II takes secondary spermatocytes to spermatids with true 1N
• Spermiogenesis


  Spermatid adds head (DNA – genetic contribution, acrosome - enzymes), midbody (mitochondria - ATP), flagellum (propulsion) mature spermatozoa
• Effects of hormones in male reproductive system


  • GnRH (Gonadotropin releasing hormone) from hypothalamus stimulates release of LH and FSH from anterior pituitary
  • LH stimulates Leydig cells to synthesize and secrete testosterone
  • Testosterone stimulates puberty, secondary sex characteristics (muscle, hair, sex organ development), sexual behavior, spermatogenesis, and protein synthesis. Negative feedback – will inhibit release of GnRH from hypothalamus and LH from anterior pituitary
  • FSH (w/ testosterone) stimulates Sertoli cells to secrete androgen binding protein (ABP, sex hormone binding globulin) which ^ testosterone concentration near seminiferous tubules
  • Inhibin – inhibits FSH secretion which slows spermatogenesis
• Accessory glands and their functions


  • Seminal vesicles – fructose provides energy for sperm to make ATP; prostaglandins improve sperm motility, viability, + female smooth muscle contraction to assist propulsion
  • Prostate gland – proteolytic enzymes to liquify semen
  • Bulbourethral/Cowper's gland – high pH, mucus fluid for lubrication of urethra and vaginal pH neutralization prior to ejaculation
• Neural mechanism for erection vs ejaculation


  1. Erection: stimuli ^ parasympathetic arterial dilation of corpus cavernosa arteries ^ blood flow erection

  2. Ejaculation: stimuli ^ sympathetic gland release of semen/fluids and muscular contraction of ejaculatory ducts ejaculation (with concurrent contraction of internal urethral sphincter to block bladder)
• Duct pathway for oocytes from formation to potential implantation or to menstrual release


  Ovary (cortex, support by the follicle) uterine tubes (swept into infundibulum by fibriae, ciliated mucosa gently carries oocyte, muscularis provides peristaltic contractions) uterus (implantation in stratum functionalis which provides support) cervix vagina (menstruation)
• Layers of the uterus


  • perimetrium – outer connective tissue
  • myometrium – smooth muscle
  • endometrium – vascularized epithelium, changes in stratum functionalis, local blood supply increases to provide nutrition to potentially implantation and support of embryo
• Oogenesis


  after puberty, primary oocyte (2N) completes Meiosis I gives a secondary oocyte (N, 2 chromatids, most cytoplasm, halted in metaphase of MII) and a polar body ovulation (release of secondary oocyte from Graafian follicle) if fertilization by sperm will undergo meiosis II ovum + 2nd polar body nuclei of sperm and ovum form 2N zygote
• Phases of the ovarian cycle


  • Follicular phase: ^ FSH ^ follicular size follicle secretes more and more estrogen matures to Graafian follicle 14th day ruptures, releases secondary oocyte = ovulation to uterine tube, if not fertilized will degenerate
  • Luteal phase: follicular cells that stay behind transform in ovary to corpus luteum - secretes progesterone and estrogen, if pregnant will help maintain uterus/endometrium, if not degenerates to corpus albicans
• Hormonal control of ovulation and corpus luteum formation


  1. hypothalamus secretes GnRH + anterior pituitary to secrete LH and FSH

  2. FSH + initial follicle growth which secretes more and more estrogen

  3. LH + further growth and maximum estrogen secretion (temporary positive feedback LH surge + ovulation, corpus luteum formation and its secretion of * progesterone and estrogen
• Effects of estrogen and progesterone


  • Estrogen - secondary sex characteristics (hips, breasts, fat), fluid/electrolyte regulation, ^ protein synthesis, lower cholesterol, moderate levels inhibit LH/FSH secretion
  • Progesterone – w/ estrogens, prepares endometrium for ovum implantation and mammary glands for milk secretion
• Corpus luteum


  Secretes progesterone and estrogen to initially support the endometrium for implantation
• Reduced corpus luteum secretion of progesterone and estrogen

  Causes vasoconstriction of uterine arteries supplying stratum functionalis which causes tissue/cell death during menstruation
• Human chorionic gonadotropin


  Embryonic hormone that helps maintain the corpus luteum
• Na/K/ATPase pump


  A primary active transport pump in the basolateral membrane of the PCT cell that uses ATP to pump sodium (Na) out of the cell and potassium (K) into the cell, creating a concentration gradient.