Renal Physiology, Hormones, and Digestive Processes

Posted on Aug 25, 2024 in Biology

Renal Hormones and Bicarbonate Reabsorption

Hormones Increasing Renal Na+ Reabsorption

1. Aldosterone

Stimulates Na+ reabsorption in principal cells of the distal convoluted tubule (DCT) and cortical collecting duct (CD) in exchange for K+.

Mechanism of Action: New protein synthesis (slow onset: 30 minutes to 2 hours). Increases the number of Na+ channels in the luminal membrane and Na+-K+ ATPase in the basolateral membrane of principal cells.

2. Angiotensin II

  1. Stimulates aldosterone secretion.
  2. In the proximal convoluted tubule (PCT): Reabsorption of Na+.

Mechanism of Action:

  • Directly stimulates Na+-K+ ATPase at the basolateral border.
  • Directly stimulates Na+-H+ countertransport at the luminal border.

Mechanism and Site of Filtered Bicarbonate Reabsorption

This process occurs in the PCT. Bicarbonate in the lumen cannot readily diffuse into tubular cells. Thus, HCO3– ions are reabsorbed by a special process:

In the Lumen

The luminal brush border of the PCT cell is the only one in renal tubules containing carbonic anhydrase (CA). H+ ions secreted into the PCT lumen by Na+-H+ exchange combine with filtered HCO3– in the presence of CA to form carbonic acid. Carbonic acid then is converted to CO2 and H2O, which diffuse into the PCT cell.

In the PCT Cells

Intracellular CA catalyzes the reaction CO2 and H2O → H2CO3 → H+ and HCO3-. H+ is secreted into the lumen via the Na+-H+ exchange mechanism in the luminal membrane, while HCO3– is reabsorbed via the basolateral membrane into the interstitium. The secreted H+ starts a new cycle.

Thus, each time an H+ ion is formed in tubular epithelial cells, an HCO3– ion is also formed and reabsorbed back into the blood. The result is net reabsorption of filtered HCO3–, but there is no net secretion of H+.

Hormones of Pregnancy

Site of Secretion

A. First Trimester (1st 3 months)

  1. Corpus luteum produces estrogen and progesterone.
  2. hCG secreted from the placenta reaches peak levels at the 7th-9th gestational week, then decreases rapidly to reach low levels and remains low during the rest of pregnancy.

B. Second & Third Trimesters

  1. Estrogen and progesterone are produced from the placenta.
  2. hPL is produced from the placenta at the 5th week of pregnancy and remains throughout it.

Functions

1. Human Chorionic Gonadotropin (hCG)

Prevents degeneration of the corpus luteum and stimulates the secretion of estrogen and progesterone by it for the maintenance of pregnancy.

2. Estrogens

  • Growth of the uterus and the mammary glands.
  • Increase the number of oxytocin receptors in the uterus.

3. Progesterone

  • Development of decidual cells needed for fetal nutrition.
  • Decreases uterine contractility during pregnancy.
  • Stimulates the growth of breast alveoli.

Both estrogen and progesterone suppress ovarian follicular growth and ovulation by inhibiting FSH & LH.

4. Human Placental Lactogen (hPL)

Similar in function to both GH and prolactin.

  • Mobilizes fat from fat stores and increases glucose production in the mother (GH effect).
  • Stimulates breast development in preparation for lactation (prolactin effect).

Gallbladder Functions and Lipid Digestion

Functions of the Gallbladder

  1. Storage of bile: Between meals, the sphincter of Oddi is closed, so bile flows to the relaxed gallbladder to be stored until needed.
  2. Concentration of bile: The volume of the gallbladder is 30-60 ml, but it can store up to 12 hours of bile secretion due to the concentration of bile caused by the absorption of water, NaCl, & bicarbonate.
  3. Acidification of bile: Due to the absorption of HCO3-, gallbladder bile becomes more acidic.

Evacuation of the Gallbladder

This occurs by the contraction of the gallbladder and the relaxation of the sphincter of Oddi.

Control of Gallbladder Evacuation

  1. CCK: The most important stimulus for gallbladder evacuation.
  2. Vagal stimulation.

Digestion of Lipids

Enzymes for Fat Digestion

  1. Gastric lipase: Digests some triglycerides to fatty acids and glycerol.
  2. Pancreatic lipase: Digests fats (triglycerides) to fatty acids & monoglycerides.
  3. Pancreatic cholesterol esterase & phospholipase: All these enzymes need bile salts to aid their digestion and emulsify the fat.

Emulsification of Fats

Bile salts reduce surface tension and emulsify fats into small droplets preparatory to their digestion by pancreatic lipases.

Factors Affecting Airway Diameter

A. Physical Factors

1. Intrapleural Pressure

The negative intrapleural pressure is the major factor keeping small airways (no cartilage) open. It distends them just as it distends alveoli.

  • With inspiration: Intrapleural pressure becomes more negative, distends airways more, airway radius becomes larger, and airway resistance decreases.
  • With expiration: The opposite occurs, increasing airway resistance.

2. Lateral Traction

Small airways have attachments to the walls of alveoli. As the alveoli expand during deep inspiration, the elastic recoil in their walls increases and is transmitted to the attachments of the airways, pulling them open and decreasing airway resistance. Thus, airway resistance decreases during inspiration and increases during expiration.

B. Nervous Factors

1. Vagus Nerve (Cholinergic) Stimulation

Causes bronchoconstriction and increased mucus secretion, increasing airway resistance.

2. β2 Adrenergic Stimulation

Causes bronchodilation.

C. Chemical Factors

Many chemical substances contract bronchial smooth muscle, e.g.:

  • Histamine: Released from mast cells during allergic responses.
  • Leukotrienes: Produced in the lungs in response to inflammation.
  • Various environmental factors.

Transport of Carbon Dioxide in Venous Blood

CO2 is generated in tissues and diffuses freely into venous blood and then into red blood cells. In red blood cells, CO2 combines with H2O to form carbonic acid, a reaction catalyzed by the enzyme carbonic anhydrase, and H2CO3 dissociates into H+ and HCO3-.

CO2 + H2O → H2CO3 → H+ + HCO3–

HCO3– leaves the red blood cells in exchange for Cl- and is transported to the lungs in the blood. H+ is buffered inside red blood cells by deoxyhemoglobin.

Dilute Urine Production in Renal Tubules

PCT

  • 2/3 of the filtered water is reabsorbed isosmotically.
  • It moves passively out of the PCT secondary to the active transport of solutes (obligatory water reabsorption).
  • Osmolarity of fluid reaching the loop of Henle is ~ 300 mOsm/L.

Thin Descending Limb of Loop of Henle

  • Permeable to water & less permeable to solutes.
  • Water is reabsorbed by osmosis, & tubular fluid reaches equilibrium with the surrounding interstitial fluid of the renal medulla.
  • Tubular fluid becomes more concentrated as it flows into the inner medulla.

Ascending Limb of Loop of Henle & Early DCT

  • Called the diluting segments as they are impermeable to water.
  • Reabsorb NaCl by Na+-K+-2Cl- cotransporter.
  • Tubular fluid becomes hyposmotic (100 mOsm/L) as it reaches the late DCT.

Late DCT & CDs

  • Additional reabsorption of solutes, especially NaCl.
  • In the absence of ADH, this portion of the tubule is impermeable to water.
  • Tubular fluid becomes even more dilute & its osmolarity is as low as 50 mOsm/L.
  • The failure to reabsorb water & the continuous reabsorption of solutes lead to a large volume of dilute urine.

Functions of the Proximal Convoluted Tubule

Reabsorption

  1. About 67% (2/3) of the filtered tubular load of Na+, Cl-, HCO3-, K+ & water.
  2. Complete reabsorption of glucose & amino acids by cotransport with Na+.
  3. Partial reabsorption of urea by diffusion, as its concentration increases in tubular fluid due to the reabsorption of water.
  4. Obligatory water reabsorption: In the PCT, the reabsorption of solutes causes the reabsorption of an equal amount of H2O, i.e., the process is isoosmotic, & the total osmolality of the tubular fluid remains unaffected (300 mOsmol).

Secretion

  1. H+ ion by Na+-H+ countertransport.
  2. Organic substances, as bile salts, urates, oxalates & catecholamines.
  3. Drugs, as penicillin, salicylates & PAH.

Connection Between Anterior Pituitary and Hypothalamus

The portal vessels connect the primary capillary plexus in the hypothalamus with the secondary capillary plexus in the anterior pituitary. Hypothalamic neurons secrete releasing & inhibitory hormones. These hormones are carried by the portal vessels from the hypothalamus to reach the anterior pituitary, thus regulating its hormones.

Hypothalamic Regulation of Prolactin

PRL is inhibited by PIH (dopamine in nature) secreted by the hypothalamus. TRH stimulates prolactin secretion. The inhibitory effect of dopamine dominates & overrides the stimulatory effect of TRH.

Actions of Prolactin

  1. Stimulates milk production in the breast. Prolactin induces the synthesis of lactose (the carbohydrate of milk), casein (the protein of milk), & lipids. It also stimulates the secretion of fluids & electrolytes by the breast.
  2. Stimulates breast development during pregnancy (with estrogen).

Actions of Oxytocin

  1. Contraction of the myoepithelial cells of the breast so milk is forced out from the mammary alveoli into the ducts & delivered to the baby (milk ejection).
  2. Contraction of the uterus: During pregnancy, oxytocin receptors in the uterus are up-regulated as labor approaches. During labor, dilation of the cervix leads to marked secretion of oxytocin & as a result, more forceful uterine contractions (positive feedback). This leads to the expulsion of the baby.
  3. Function in males: Contraction of the vas deferens & propelling of sperm to the urethra.

Ovarian Changes in the First Week of the Follicular Phase

Follicular Phase

From day 0 till day 14. The variability in the length of the cycle is attributable to variability in the duration of this phase.

Ovarian Changes During the First Week

  1. Due to increased levels of FSH & to a lesser extent LH secreted from the anterior pituitary, 10-15 primordial follicles start growing. This occurs by the enlargement of the ovum itself 2-3x with the proliferation of granulosa cells (primary follicle).
  2. Granulosa cells secrete glycoprotein material called zona pellucida. Also, stromal cells develop around granulosa cells & they are called theca cells. The theca cells divide into secretory theca interna & an outer rim of fibrous tissue called theca externa (preantral follicles).
  3. Granulosa cells contain FSH receptors & theca interna cells contain LH receptors.
  4. Increased FSH & LH will lead to the multiplication of granulosa & theca cells so the follicles increase in size & fluid collects between granulosa cells forming a large cavity filled with fluid called antrum (antral follicles).

Estrogen Formation by the Growing Follicles

LH stimulates theca interna cells to produce androgens & in the presence of FSH, these androgens are converted by granulosa cells to estrogens which accumulate in the antral fluid or are secreted in the blood.

Buffering of Hydrogen Ions in Renal Tubular Fluid

In PCT

In the Lumen

In the presence of CA, secreted H+ & filtered HCO3– form carbonic acid, which then is converted to CO2 & H2O, which diffuse into the PCT cell.

In the PCT Cells

In the presence of CA, CO2 & H2O → H2CO3 → H+ & HCO3-. H+ is secreted into the lumen via the Na+-H+ exchange mechanism in the luminal membrane, while HCO3– is reabsorbed via the basolateral membrane into the interstitium. The secreted H+ starts a new cycle. Thus, each time an H+ ion is formed in tubular epithelial cells, an HCO3– ion is also formed and reabsorbed back into the blood. The result is net reabsorption of filtered HCO3-, but there is no net secretion of H+.

In Late DCT & CD

1. Excretion of H+ as Titratable Acid (H2PO4-)

In Tubular Cells

H+ & HCO3– are produced in the cell from CO2 & H2O. The H+ is secreted into the lumen & the HCO3– is reabsorbed into the blood (“new” HCO3-).

In the Tubular Lumen

The secreted H+ combines with filtered HPO42- to form H2PO4-, which is excreted as titratable acid. This process results in net secretion of H+ & net reabsorption of newly formed HCO3-. As a result of H+ secretion, the pH of urine becomes progressively lower.

2. Excretion of H+ as Ammonium (NH4+)

In Tubular Cells

NH3 (ammonia) is produced by renal cells from glutamine. It diffuses down its concentration gradient from the cells into the lumen. H+ & HCO3– are produced from CO2 & H2O. The H+ ion is secreted into the lumen, while the HCO3– ion is reabsorbed into the blood (“new” HCO3-).

In Lumen

H+ combines with NH3 to form NH4+, which is excreted. This process also results in net secretion of H+ & net reabsorption of newly synthesized HCO3-.

Autoregulation and Glomerulotubular Balance

Autoregulation

Keeps the GFR constant over the range of ABP 80 – 200 mmHg by changing the renal vascular resistance.

1. Myogenic Autoregulation

The renal arterioles contract in response to stretch. Thus, decreased ABP stretches the arterioles, which contract, increasing vascular resistance and preventing a decrease in GFR during decreased ABP.

2. Tubuloglomerular Feedback

A feedback mechanism that buffers the effect of increased ABP on GFR:

Increased ABP → Increased GFR → Slow rate of flow of tubular fluid in renal tubules → Decreased NaCl reabsorption in the loop of Henle → Decreased NaCl concentration in tubular fluid reaching the DCT → Initiates a signal in the macula densa that has two effects:

  • Vasodilation in the afferent arteriole: Decreases PGC and decreases GFR toward normal.
  • Vasoconstriction of the efferent arteriole (indirectly): Renin release by juxtaglomerular cells → Angiotensin II → Vasoconstriction of the efferent arteriole → Decreases PGC and prevents a decrease in GFR during decreased ABP.

Glomerulotubular Balance

Importance

Represents the ability of the PCT to reabsorb a constant fraction (2/3 or 67%) of the filtered load of Na+ & water. It helps prevent overloading of distal tubular segments when GFR increases.

Mechanism

Glomerulotubular balance is based on Starling forces in peritubular capillaries, which alter Na+ & H2O reabsorption: A decrease in GFR results in a decrease in protein concentration and oncotic pressure (decreased PC), as well as an increase in hydrostatic pressure (increased PC) of peritubular capillaries. This, in turn, causes a decrease in water reabsorption from the PCT. Since water reabsorption is accompanied by Na+ reabsorption, there is matching filtration & reabsorption or glomerulotubular balance.

Tubuloglomerular Feedback

Importance

A feedback mechanism that buffers the effect of decreased ABP on GFR.

Mechanism

Decreased ABP → Decreased GFR → Slow rate of flow of tubular fluid in renal tubules → Decreased NaCl reabsorption in the loop of Henle → Decreased NaCl concentration in tubular fluid reaching the DCT → Initiates a signal in the macula densa that has two effects:

  • Vasodilation in the afferent arteriole: Decreases PGC and decreases GFR toward normal.
  • Vasoconstriction of the efferent arteriole: Decreased renin release by juxtaglomerular cells → Decreased Angiotensin II → Vasoconstriction of the efferent arteriole → Decreases PGC and prevents a decrease in GFR during decreased ABP.

Water Reabsorption in the Presence of ADH

PCT

67% of the filtered water is reabsorbed isosmotically. It moves passively out of the PCT secondary to the active transport of solutes (obligatory water reabsorption).

Thin Descending Limb of Loop of Henle

Permeable to water & less permeable to solutes. Water is reabsorbed by osmosis & tubular fluid reaches osmotic equilibrium with the surrounding interstitial fluid of the renal medulla.

Ascending Limb of Loop of Henle & Early DCT

Called the diluting segments. They are impermeable to water. They reabsorb NaCl by Na+-K+-2Cl- cotransporter.

Late DCT & CDs

ADH increases the water permeability of the principal cells of the late DCT & CDs. Water is reabsorbed until the osmolarity of the DCT equals that of the surrounding interstitial fluid in the renal cortex. As the tubular fluid flows through the CDs, it passes through regions of increasing hyperosmolarity toward the inner medulla. Water is reabsorbed from the CDs until the osmolarity of the tubular fluid equals that of the surrounding interstitial fluid.

Estrogen and Progesterone Sources and Functions

Sources of Estrogen and Progesterone

  1. In the 1st trimester, they are secreted by the corpus luteum.
  2. In the 2nd & 3rd trimesters, they are produced by the placenta.

Function of Progesterone During Pregnancy

  1. Development of decidual cells needed for fetal nutrition.
  2. Decreases uterine contractility during pregnancy.
  3. Stimulates growth of the breast alveoli.

Function of Estrogen in the Initiation of Labor

  1. During the last weeks of pregnancy, as a result of the increasing levels of estrogen, the smooth muscle cells synthesize connexin, proteins that form gap junctions between cells, which allow the myometrium to contract coordinated contractions as one unit.
  2. Simultaneously, the cervix becomes soft & flexible due to enzymatically mediated breakup of collagen fibers. The synthesis of these enzymes is mediated by estrogen & placental prostaglandins.
  3. Increases the number of oxytocin receptors in the uterus.

Functions of Estrogen in Nonpregnant Females

1. Development of Secondary Sex Characteristics

  • Deposition of fat in the subcutaneous tissues, especially in the breasts, thighs & buttocks.
  • Narrow shoulders, broad hips, less body hair & more scalp hair.
  • High pitched voice.

2. Actions on Growth

  • Stimulates linear growth of bones at puberty (pubertal spurt of growth).
  • Causes early closure of the epiphysis so that girls stop growing in height several years before boys of the same age group.

Obstructive Jaundice and Lipid Digestion

Obstructive Jaundice

The patient is suffering from obstructive jaundice due to obstruction in the bile flow by stones or cancer.

Absorption of Lipids

  1. Micelle formation: Bile salts are amphipathic, i.e., one surface is hydrophilic & the other is hydrophobic. Thus bile salts tend to form cylindrical discs called micelles, with the hydrophilic surface facing out & a hydrophobic center containing fats. Thus, micelles keep fats in solution & transport them to the brush border of the small intestine where they are absorbed.
  2. In the intestinal cell: The products of lipid digestion are re-esterified to triglycerides, cholesterol ester & phospholipids & then together with protein from the cell they form chylomicrons.
  3. Chylomicrons: Are transported out of the intestinal cell by exocytosis. Because they are too large to enter the capillaries, they enter the lymph vessels.

Digestion of Lipids

Enzymes for Fat Digestion

  1. Gastric lipase: Digests some triglycerides to fatty acids and glycerol.
  2. Pancreatic lipase: Digests fats (triglycerides) to fatty acids & monoglycerides.
  3. Pancreatic cholesterol esterase & phospholipase: All these enzymes need bile salts to aid their digestion and emulsify the fat.

Emulsification of Fats

Bile salts reduce surface tension and emulsify fats into small droplets preparatory to their digestion by pancreatic lipases.

Migrating Motor Complex (MMC)

Characteristics

  1. Occurs during fasting between meals & is immediately stopped by the ingestion of food.
  2. Consists of repeated waves of peristaltic activity that travel a short distance along the small intestine then die out.
  3. Each new wave starts slightly lower than the previous one. Thus the waves slowly migrate down the small intestine, taking about 2 hours to reach the large intestine.

Functions of MMC

  1. Moves any undigested substances still remaining in the small intestine to the large intestine.
  2. Prevents bacteria from remaining in the small intestine long enough to grow & multiply excessively.

Mechanism of Gastric HCl Secretion and Stimulants

Mechanism of HCl Secretion

  1. Cl- is actively transported from the cytoplasm to the lumen. This creates a negative potential of -40 to -70 mV inside the lumen.
  2. This leads to the passive diffusion of K+ from the cell to the lumen.
  3. H2O dissociates into H+ & OH- in the cell cytoplasm.
  4. H+ is actively secreted to the lumen in exchange for K+ by the H+/K+ ATPase pump (proton pump). Thus, most of the K+ that had diffused into the lumen in step 2 is reabsorbed by the cell & H+ takes their place in the lumen.
  5. CO2 (formed during cell metabolism or entering by blood) combines with H2O under the effect of carbonic anhydrase enzyme to form carbonic acid.
  6. Carbonic acid dissociates into HCO3– & H+.
  7. H+ combines with OH- released in step 3 to form H2O. The HCO3– diffuses out of the cell in exchange for Cl- then step 1 is repeated.
  8. H2O passes through the cell to the lumen by osmosis.

Stimulants of Acid Secretion

  1. Acetylcholine
  2. Gastrin hormone
  3. Histamine

Mechanism of Action of Stimulants

Parietal cells contain receptors for these stimuli. Binding of stimuli with the receptors releases second messengers which transfer the H+/K+ ATPase proteins from the intracellular vesicles to the cell luminal membrane.

1. Acetylcholine

Acts via M3 muscarinic receptors. It releases intracellular Ca2+ as a second messenger.

2. Gastrin

Acts by two ways:

  • Directly via gastrin receptors on parietal cells. This increases intracellular Ca2+ as a second messenger.
  • Indirectly through stimulating the secretion of histamine.

3. Histamine

Acts via H2 receptors. H2 receptor stimulation increases intracellular cAMP as a second messenger. It is very important because it acts by a different second messenger & it potentiates the action of other two stimuli.

Role of Prostaglandins and Stages of Labor

Role of Prostaglandins

  1. Stimulate uterine contractions.
  2. Increase the action of oxytocin on uterine muscles.
  3. Stimulate the synthesis of enzymes that break collagen fibers & soften the cervix.

Stages of Labor

1st Stage

  1. Includes dilation of the cervix & initiation of regular uterine contractions.
  2. Begins from the onset of labor to full dilation of the cervix (reaches 10 cm).
  3. The amniotic sac ruptures at the onset of parturition or before.

2nd Stage

  1. Includes the expulsion of the baby from the birth canal.
  2. Begins from the full dilation of the cervix to total expulsion of the baby.

3rd Stage

  1. Includes the expulsion of fetal membranes & placenta after its separation.
  2. During 10-45 minutes after the birth of the baby, the uterus contracts to a very small size. This causes the separation of the placenta from its implantation site.

Prolactin Hormone and Uterine Changes

Prolactin Hormone

  1. Responsible for milk formation. During pregnancy, its level increases steadily because estrogen stimulates its secretion.
  2. Prolactin & estrogen together stimulate breast growth but lactation does not occur because estrogen antagonizes the milk-producing effect of prolactin on the breast.
  3. After labor, estrogen levels decrease. This causes a decrease in prolactin levels which reaches non-pregnant levels.
  4. Each time the mother nurses her baby, suckling stimulates prolactin secretion. Thus there are large secretory bursts of prolactin during each nursing period.

Uterine Changes During the Luteal Phase

  1. After ovulation, the increased progesterone stimulates the secretion of the endometrial glands which become coiled.
  2. It also stimulates the development of blood vessels which become coiled.
  3. Progesterone stimulates glycogen deposition in the endometrium.
  4. The endometrium becomes 6-7 mm in thickness.

Urea Recycling and Mechanisms of Renal Function

Urea Recycling

& its physiologic significance.a.mechanism: – ascending limb of loop of henle,dct,cortical cds & outer medullary cds R impermeable 2 urea.- as w8r is reabsorbed frm l8 dct,cortical & outer medullary cds,urea concentr8on ­ rapidly.- in inner medullary cds,further w8r reabsorption takes place,so dat urea concentr8on rises even more.thus,urea diffuses out of d tubule in2 renal interstitium coz dis segment is highly permeable 2 urea,& adh increases dis permeability even more.- a moder8 share of d urea dat moves in2 medullary interstitium,diffuses in2 thin descending limb of loop of henle,so dat it passes again in tubular fluid.  it recircul8s several times be4 it is excreted.each time around it contributes 2 a higher concentr8on of urea in interstitium.significance: urea recircul8on provides an additional mechanism 4 4ming a hyperosmotic medulla.in d presence of adh,urea contibutes 40% 2 d medullary interstitial osmolarity (= 500 mosm/l). 

2.describe d mechanisms of glomerulotubular balance & tubulo-glomerular feedback.  ? is their importance?glomerulotubular balance: importance: it represents d ability of d pct 2 reabsorb a constant fraction (2/3 or 67%) of d filtered load of na+ & w8r.  it helps prevent overloading of distal tubular segments wen gfr ­.mechanism: glomerulotubular balance is based on starling 4ces in peritubular capillaries,which alter na+ & h2o reabsorption: ­ in gfr results in ­ in protein conc.& oncotic pressure (­ pc),as well as a ¯ hydrost8c pressure (¯ pc) of peritubular capillaries.  dis,in turn,causes an ­ in w8r reabsorption frm pct. since w8r reabsorption is accompanied by na+ reabsorption,there is matching filtr8on & reabsorption or glomerulotubular balance.tubuloglomerular feedback: importance: it is a feedback mechanism dat buffers d effect of ¯ abp on gfr.mechanism:¯ abp ® ¯ gfr ® slow r8 of flow of tubular fluid in renal tubules ® ­ nacl reabsorption in loop of henle ® ¯ nacl conc.in tubular fluid reaching d dct ® initi8s a signal in macula densa dat hs 2 effects:a.vd in afferent arteriole: ® ­ pgc ® ­ gfr 2ward normal.  b.vc of efferent arteriole: ­ renin release by juxta-glomerular cells ® ­ @ ii ® vc of efferent arteriole ® ­ pgc ® prevents ¯ gfr during ¯ abp.


b- w8r reabsorption in d presence of adh:pct: 67% of d filtered w8r is reasorbed isosmotically. it moves passively out of pct 2ry 2 active transport of solutes (obliga2ry w8r reabsorption).thin descending limb of loop of henle: it is permeable 2 w8r & less permeable 2 solutes.  w8r is reabsorbed by osmosis & tubular fluid reaches osmotic equilibrium with surrounding interstitial fluid of renal medulla.ascending limb of loop of henle & early dct: dey R called d diluting segments. dey R impermeable 2 w8r.dey reabsorb nacl by na+-k+-2cl– cotransporter.l8 dct & cds:  adh increases d w8r permeability of d principal cells of d l8 dct & cds.w8r is reabsorbed til d osmolarity of d dct equals dat of surrounding interstitial fluid in renal cortex.as d tubular fluid flows thru d cds,it passes thru regions of increasing hyperosmolarity 2ward d inner medulla.w8r is reabsorbed frm d cds til d osmolarity of d tubular fluid equals dat of d surrounding interstitial fluid. 


a-d different sources of estrogen & progester1:1- in d 1st trimester dey R secreted by d corpus luteum2- in d 2nd & 3rd trimesters dey R produced by d placenta.

b- d function of progester1 during pregnancy:1- development of decidual cells needed 4 fetal nutrition.2- decreases uterine contractility during pregnancy.         3- stimul8s growth of d breast alveoli.

c- d function of estrogen in d initi8on of labor:1- during d last weeks of pregnancy as a result of d increasing levels of estrogen,d smooth muscle cells synthesize connexin,proteins dat 4m gap junctions btwn cells,which allow d myometrium 2 contract coordin8d contractions as 1 unit.2- simultaneously,d cervix becomes soft & flexible due 2 enzym8cally medi8d breakup of collagen fibers.d synthesis of these enzymes is medi8d by estrogen & placental prostaglandins.3- increases d # of oxy2cin recep2rs in d uterus.

d- d 2 functions of estrogen in d nonpregnant females:1- development of secondary sex characteristics: a- deposition of fat in d subcutaneous tissues especially in d breasts,thigh & but2cks.b- narrow shoulders,broad hips,less body hair & more scalp hair.c- hi pitched voice.2- actions on growth: a- it stimul8s linear growth of b1s @ puberty (pubertal spurt of growth).b- it causes early closure of d epiphysis so dat d girls s2p growing in h8 several years be4 d boys of d same age group.


a- a female p8ent is suffering frm yellow discolor8on of d skin & mucus membrane.her blood analysis showed dat d level of conjug8d bilirubin exceeds 4 mg%.d p8ent complained of fatty s2ols.a)1- d p8ent is suffering frm obstructive jaundice due 2 obstruction in d bile flow by st1s or cancer.

2- absorption of lipids:1– micelle 4m8on:bile salts R amphipathic,i.e.,1 surface is hydrophilic & d other is hydrophobic.thus bile salts tend 2 4m cylindrical discs called micelles,with d hydrophilic surface facing out & a hydrophobic center containing fats.thus,micelles keep fats in solution & transport dem 2 d brush border of    d small intestine where dey R absorbed.2– in d intestinal cell,d products of lipid digestion R reesterified 2 triglycerides,cholesterol ester & phospholipids & then 2gether with protein frm d cell dey 4m chylomicrons.3– chylomicrons R transported out of d intestinal cell by exocy2sis.coz dey R 2o large 2 enter d capillaries dey enter d lymph vessels.digestion of lipids:enzymes 4 fat digestion:1- gastric lipase: digest some triglycerides 2 fatty acids & glycerol.2- pancre8c lipase which digest fats (triglycerides) 2 fatty acids & monoglycerides.3- pancre8c cholesterol esterase & phospholipase.ol these enzymes nid bile salts 2 aid their digestion & emulsify d fat.emulsific8on of fats:bile salts reduce surface tension & emulsify fats in2 small droplets prepara2ry 2 their digestion by pancre8c lipases.

b.d migr8ng mo2r complex (mmc):1- it occurs during fasting btwn meals & is immedi8ly s2pped by d ingestion of food.2- it consists of repe8d waves of peristaltic activity dat travel a short distance along d small intestine then die out.3- each new wave starts slightly lower than d previous 1.thus d waves slowly migr8 down d small intestine taking about 2 hours 2 reach d large intestine.functions of mmc:1- it moves ne undigested substances still remaining in small intestine 2 large intestine.2- it prevents bacteria frm remaining in d small intestine long enough 2 grow & multiply excessively.