LECTURE OUTLINE - PHYSIOLOGY OF THE KIDNEYS

KNOW BASIC ANATOMYGROSS STRUCTURE & MICROSCOPIC STRUCTURE

PROCESS OF URINE FORMATION1) GLOMERULUS FILTRATION

(intrinsic and extrinsic controls)2) TUBULAR REABSORPTION

(FROM TUBULES)3) TUBULAR SECRETION

(INTO TUBULES)

STUDY MECHANISM OF EACH

WHAT IS ABSORBED AND IN WHAT PART

COUNTERCURRENT MULTIPLIER SYSTEM

ADH COLLECTING DUCT EFFECT

RENAL CLEARANCE OF INULIN AND CREATINE

CLEARANCE OF UREA

RENAL CONTROL OF ELECTROLYTE BALANCE

RENAL CONTROL OF ACID-BASE BALANCE

LECTURE OUTLINE CONTINUED

Membrane Junctions

Tight junction – impermeable junction that encircles the cell

Desmosome – anchoring junction scattered along the sides of cells

Gap junction – a nexus that allows chemical substances to pass between cells

Membrane Junctions: Tight Junction

Figure 3.5a

Membrane Junctions: Desmosome

Figure 3.5b

Membrane Junctions: Gap Junction

Figure 3.5c

Continuous Capillaries

Figure 19.3a

Continuous Capillaries

Continuous capillaries of the brain:

Have tight junctions completely around the endothelium

Constitute the blood-brain barrier

Fenestrated Capillaries

Figure 19.3b

Fenestrated Capillaries

Found wherever active capillary absorption or filtrate formation occurs (e.g., small intestines, endocrine glands, and kidneys)

Characterized by:

An endothelium riddled with pores (fenestrations)

Greater permeability to solutes and fluids than other capillaries

Sinusoids

Highly modified, leaky, fenestrated capillaries with large lumens

Found in the liver, bone marrow, lymphoid tissue, and in some endocrine organs

Allow large molecules (proteins and blood cells) to pass between the blood and surrounding tissues

Blood flows sluggishly, allowing for modification in various ways

Sinusoids

Figure 19.3c

Mechanisms of Urine Formation

Urine formation and adjustment of blood composition involves three major processes

Glomerular filtration

Tubular reabsorption

SecretionFigure 25.8

Kidney Functions

Filter 180 liters (45 gallons) of blood daily, allowing toxins, metabolic wastes, and excess ions to leave the body in urine

Regulate volume and chemical makeup of the blood

Maintain the proper balance between water and salts, and acids and bases

Other Urinary System Organs

Urinary bladder – provides a temporary storage reservoir for urine

Paired ureters – transport urine from the kidneys to the bladder

Urethra – transports urine from the bladder out of the body

Internal Anatomy

Figure 25.3b

Blood Supply

Approximately one-fourth (1200 ml) of systemic cardiac output flows through the kidneys each minute

Arterial flow into and venous flow out of the kidneys follow similar paths

Figure 25.3c

The Nephron

Figure 25.4b

Nephrons

Figure 25.5b

Vascular Resistance in Microcirculation

Afferent and efferent arterioles offer high resistance to blood flow

Blood pressure declines from 95mm Hg in renal arteries to 8 mm Hg in renal veins

Juxtaglomerular Apparatus (JGA)

Figure 25.6

Filtration Membrane

Figure 25.7a

Filtration Membrane

Figure 25.7c

Mechanisms of Urine Formation

Urine formation and adjustment of blood composition involves three major processes

Glomerular filtration

Tubular reabsorption

SecretionFigure 25.8

Glomerular Filtration

Principles of fluid dynamics that account for tissue fluid in all capillary beds apply to the glomerulus as well

The glomerulus is more efficient than other capillary beds because:

Its filtration membrane is significantly more permeable

Glomerular blood pressure is higher

It has a higher net filtration pressure

Plasma proteins are not filtered and are used to maintain osmotic pressure of the blood

Net Filtration Pressure (NFP)

The pressure responsible for filtrate formation

NFP equals the glomerular hydrostatic pressure (HPg) minus the osmotic pressure of glomerular blood (OPg) combined with the capsular hydrostatic pressure (HPc)

NFP = HPg – (OPg + HPc)

BLOOD IS FILTERED BY:A) Hydrostatic pressure (heart) +55 mmHg

Capsule pressure–15

mmHg(materials inside)

Colloid pressure–30

mmHg (elements of the blood

plasma)~osmotic pressure of solutes

55 – 45 = approx 10 mmHgTHIS IS THE NET FILTRATION PRESSURE!!

Exam questions:

What would an increase in blood pressure do?What effect would this have on urine production?

Glomerular Filtration Rate (GFR)

Figure 25.9

Glomerular Filtration Rate (GFR) inBowmans’s capsule CAPSULE

BOWMAN’S CAPSULE The total amount of filtrate formed per minute by the kidneys

≈ 125 ml of fluid per min (men)

≈ 120 ml of fluid per min (women)

THIS IS CALLED GFR OR

GLOMERULAR FILTRATION RATE

ULTRAFILTRATE

(formed under pressure ≈ 10mmHg)

≈ 125 ml of fluid per min (men) ≈ 7.5 liters per hr OR 180 liters per day ≈ 45 gallons of fluid

Glomerular Filtration Rate (GFR) inBowmans’s capsule continued CAPSULE

BOWMAN’S CAPSULE

TOTAL BLOOD VOLUME IS 5.5 liters

Therefore total blood volume is filtered into the glomerulus (and ends up in Bowman’s capsule) every 40 minutes

PROBLEM??

WATER, SALTS, GLUCOSE ETC. ALL NEED TO BE REABSORBED!!!

about 99% of the filtrate (formative urine) is

REABSORBED

Glomerular Filtration Rate (GFR)

GFR is directly proportional to the NFP

Changes in GFR normally result from changes in glomerular blood pressure

Regulation of Glomerular Filtration

If the GFR is too high:

Needed substances cannot be reabsorbed quickly enough and are lost in the urine

If the GFR is too low:

Everything is reabsorbed, including wastes that are normally disposed of

Regulation of Glomerular Filtration

Three mechanisms control the GFR

Renal autoregulation (intrinsic system)

Neural controls

Hormonal mechanism (the renin-angiotensin system)

Renal autoregulation (intrinsic system)

REGULATION OF GFR

GFR RATE IS UNDER HOMEOSTATIC CONTROL

VASOCONSTRICTION OR VASODILATION OF AFFERENT ARTERIOLES (intrinsic factors)

KNOWN AS MYOGENIC RENAL AUTOREGULATION

(Myogenic – responds to changes in pressure in the renal blood vessels)

Renal autoregulation (intrinsic system)

FR

LOW BLOOD PRESSURE ——> vasodilation

greater blood flow ——> increased GFR

HIGH BLOOD PRESSURE ——> vasoconstriction

reduced blood flow ———> decreased GFR

MAINTAINS WATER AND SOLUTE FILTRATION

Under normal conditions, renal autoregulation maintains a nearly constant glomerular filtration rate

Extrinsic Controls

When the sympathetic nervous system is at rest:

Renal blood vessels are maximally dilated

Autoregulation mechanisms prevail

Extrinsic Controls

Decrease in blood pressure ----> baroreceptors in aorta

----> increased sympathetic nerve activity ------>

1) vasoconstriction of GI tract and skin

2) heart rate increased (therefore cardiac output)

-----> BOTH raise systemic blood pressure

Extrinsic Controls

Under stress:

Norepinephrine/epinephrine is released by the sympathetic nervous system

Epinephrine is also released by the adrenal medulla

Afferent arterioles constrict and filtration is inhibited

Juxtaglomerular Apparatus (JGA)

Figure 25.6

Renin Release

Renin release is triggered by:

1) Reduced stretch of the granular JG cells

Stimulus (low blood pressure; therefore

reduced blood flow to kidneys)

2) Direct stimulation of the JG cells via

noreepinephrine/epinephrine by renal nerves

Renin Release

WHICH STIMULATES CELLS IN JUXTAGLOMERULUS APPARATUS

——> RELEASES RENIN ——>

TRAVELS TO LIVER ——>

STIMULATES RELEASE OFANGIOTENSINOGEN ——>

TRAVELS IN BLOOD TO LUNGS ——>

CONVERTS ANGIOTENSIN I TO ANGIOTENSIN II

Renin-Angiotensin Mechanism

Is triggered when the JG cells release renin

Travels to liver

Renin releases angiotensinogen

Angiotensinogen converted to angiotensin I

Angiotensin I travels in blood to lungs and is converted to angiotensin II

Angiotensin II action (s):

ANGIOTENSIN II

ACTS ON FOUR (4) DIFFERENT EFFECTORS

1. VASOCONSTRICTION OF SYSTEMIC ARTERIOLES (INCREASES BLOOD PRESSURE)

2. STIMULATES ALDOSTERONE SECRETION FROM ADRENAL CORTEX

ALDOSTERONE ————> INCREASES WATER RETENTION OF SODIUM, CHLORIDE AND WATER BY KIDNEYS ————> INCREASES BLOOD VOLUME ————> INCREASES BLOOD PRESSURE

3. STIMULATION OF THIRST CENTERS IN HYPOTHALAMUS

(CAUSES INCREASED WATER INTAKE ———> INCREASES BLOOD VOLUME ——> INCREASES BLOOD PRESSURE!!

4. STIMULATION OF ADH FROM POSTERIOR PITUITARY GLAND

ADH PROMOTES WATER RETENTION BY KIDNEYS

(makes distal tubule and collecting ducts more permeable to water) ———> INCREASES BLOOD VOLUME ———> INCREASES BLOOD PRESSURE!!

(ALL 4 EFFECTORS WILL RETURN GFR BACK TO “NORMAL”)

ATRIAL NATRIURETIC PEPTIDE (ANP)

(cells discovered in left and right atria in 1983)

Stretching of cells due to INCREASED BLOOD VOLUME

(INCREASED BLOOD PRESSURE)

PROMOTES EXCRETION OF WATER (DIURESIS)

AND EXCRETION OF SODIUM (NATRIURESIS)

HOW??

1. DILATES AFFERENT ARTERIOLES (INCREASES GFR)

2. INCREASES PERMEABILITY OF GLOMERULUS (INCREASES GFR)

3. DECREASES ADH

4. DECREASES ALDOSTERONE

5. DECREASES RENIN

(a decrease in blood volume as a result of 1 through 5 inhibits

Cells in Left and Right Atria)

Renin Release

Figure 25.10

Osmotic Gradient in the Renal Medulla

Figure 25.13