Transcript of Chapter 29: Renal Regulation of K, Ca, P, and Mg; Integration of Renal Mechanisms for Control of...
- Slide 1
- Chapter 29: Renal Regulation of K, Ca, P, and Mg; Integration
of Renal Mechanisms for Control of Blood Volume and ECF Volume
Guyton and Hall, Textbook of Medical Physiology, 12 th edition
- Slide 2
- Regulation of ECF Potassium Concentration and Excretion
Regulation of Internal K Distribution a.Insulin stimulates K uptake
into cells b.Aldosterone increases K uptake into cells
c.Beta-adrenergic stimulation increases cellular uptake d.Acid-base
abnormalities changes distribution e.Cell lysis causes increased
extracellular K concentration f.Strenuous exercise causes
hyperkalemia by releasing K from skeletal muscles g.Increased ECF
osmolarity causes redistribution of K from cells to the ECF
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- Fig. 29.1 Normal potassium intake, distribution of potassium in
the body fluids, and potassium output from the body
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- Factors That Shift K into Cells and Decrease Extracellular K
Concentration Factors That Shift K out of Cells and Increase
Cellular K Concentration InsulinInsulin deficiency (diabetes)
AldosteroneAldosterone deficiency (Addisons) Beta-adrenergic
stimulationBeta-adrenergic blockade AlkalosisAcidosis Cell lysis
Strenuous exercise Increased ECF osmolarity Table. 29.1 Factors
that can alter potassium distribution between the intracellular and
extracellular fluids
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- Overview of Renal Potassium Excretion Renal Potassium
Excretion- determined by the sum of three processes a.The rate of K
filtration (GFR X plasma K conc. b.The rate of K reabsorption by
the tubules c.The rate of K secretion by the tubules
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- Overview of Renal Potassium Excretion Fig. 29.2
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- Overview of Renal Potassium Excretion (cont.) Fig. 29.3 K
Secretion by Principal Cells of Late Distal and Cortical Collecting
Tubules
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- Summary of Factors That Regulate Potassium Increased ECF
Potassium Concentration Stimulates Potassium Secretion Fig.
29.4
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- Summary of Factors That Regulate Potassium Aldosterone
Stimulates Potassium Secretion Increased Extracellular Potassium
Ion Concentration Stimulates Aldosterone Secretion Fig. 29.5
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- Fig. 29.6 Basic feedback mechanism for control of ECF potassium
concentration by aldosterone
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- Fig. 29.7 Primary mechanisms by which high potassium intake
raises potassium excretion
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- Summary of Potassium Regulation (cont.) Blockade of Aldosterone
Feedback System Impairs Control of Potassium Concentration Fig.
29.8
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- Summary of Potassium Regulation (cont.) Increased Distal
Tubular Flow Rate Stimulates Potassium Secretion Fig. 29.9
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- Fig. 29.10 Effect of high sodium intake on renal excretion of
potassium
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- Control of Renal Calcium Excretion and Extracellular Calcium
Ion Concentration 50% of plasma calcium is in ionized form Intake
must be balanced with net loss 99% of the bodys calcium is stored
in bone Bone, therefore, is the primary reservoir of calcium PTH is
one of the most important regulators of calcium release
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- Control of Renal Calcium Excretion and Extracellular Calcium
Ion Concentration PTH regulates through 3 main effects
a.Stimulating bone resorption b.Stimulate activation of vitamin D
which increases intestinal reabsorption of calcium c.Directly
increasing renal tubular calcium reabsorption
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- Control of Renal Calcium Excretion and Extracellular Calcium
Ion Concentration Fig. 29.11 Compensatory responses to decreased
plasma ionized calcium concentration mediated by parathyroid
hormone (PTH) and vitamin D
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- Control of Calcium Excretion By the Kidneys Proximal Tubular
Calcium Reabsorption a.Most occurs through the paracellular pathway
dissolved in water b.20% occurs through a transcellular
pathway
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- Control of Calcium Excretion By the Kidneys Fig. 29.12
Mechanisms of calcium reabsorption by paracellular and
transcellular pathways in the proximal tubular cells
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- Control of Calcium Excretion By the Kidneys Loop of Henle and
Distal Tubule Calcium Reabsorption a.Restricted to the thick
ascending limb of the Loop b.Almost entirely by active transport in
the distal tubule
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- Control of Calcium Excretion By the Kidneys Factors That
Regulate Tubular Calcium Reabsorption Decreased Ca
ExcretionIncreased Ca Excretion Increased Parathyroid
hormoneDecreased Parathyroid hormone Decreased ECF volumeIncreased
ECF volume Decreased blood pressureIncreased blood pressure
Increased plasma phosphateDecreased plasma phosphate Metabolic
acidosisMetabolic alkalosis Vitamin D 3 Table. 29.2 Factors that
alter renal calcium excretion
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- Regulation of Renal Phosphate Excretion Proximal tubule
normally reabsorbs 75-80% of the filtered phosphate Distal tubule
reabsorbs approx. 10% 10% excreted through the urine When plasma
PTH is increased, phosphate reabsorption is decreased and excretion
is increased
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- Regulation of Renal Magnesium More than 50% of the bodys Mg is
stored in bones Primary reabsorption site is the loop of Henle
Following lead to increased Mg excretion: a.Increased ECF Mg
concentration b.ECF expansion c.Increased ECF Ca concentration
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- Regulation of Sodium Sodium Intake and Excretion are Matched
Under Steady-State Conditions Sodium Excretion is Controlled by
Altering GFR or Tubular Na reabsorption rate
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- Regulation of Sodium Importance of Pressure Natriuresis and
Pressure Diuresis in Maintaining Body Na and Fluid Balance Fig.
29.13 Acute and chronic effects of arterial pressure on sodium
output by the kidneys (pressure natriuresis)
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- Regulation of Sodium Pressure Natriuresis and Diuresiskey
components of feedback mechanism for regulating body fluid volumes
and arterial pressure Fig. 29.14
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- Fig. 29.15 Approximate effect of changes in daily fluid intake
on blood volume
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- Precision of Blood Volume and ECF Volume Regulation Blood
volume remains almost exactly constant despite extreme changes in
daily fluid intake (Fig. 29.14); the reason is a.A slight change in
blood volume causes a marked change in cardiac output b.A slight
change in CO causes a large change in blood pressure c.A slight
change in BP causes a large change in urine output
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- Distribution of ECF Fig. 29.16 Approximate relation between ECF
and blood volume
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- Distribution of ECF Principal Factors That Can Cause
Accumulation of Fluid in Interstitial Spaces a.Increased capillary
hydorstatic pressure b.Decreased plasma colloid osmotic pressure
c.Increased permeability of the capillaries d.Obstruction of
lymphatic vessels
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- Nervous and Hormonal Factors Increase the Effectiveness of
Renal-Body Fluid Feedback Control SNS Control of Renal Excretion:
arterial baroreceptor and low-pressure stretch receptor reflexes
Role of Angiotensin II in Controlling Renal Excretion a.When Na
intake is elevated above normal, renin secretion is decreased,
causing decreased angiotensin II formation b.When Na intake is
reduced below normal, increased angiotensin II causes Na and water
retention
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- Fig. 29.17 Effects of excessive angiotensin II formation and
blocking angiotensin II formation on the renal pressure natriuresis
curve Importance of Changes in Angiotensin II in Altering Pressure
Natriuresis
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- Angiotensin II (cont.) Excessive Angiotensin IIdoes not usually
cause large increases in ECF volume Increased Arterial Pressure
Counterbalances Angiotensin II Mediated Sodium Retention
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- Role of Aldosterone in Renal Excretion Aldosterone Increases
Sodium Reabsorption Reduction in Sodium Intake- increased
angiotensin II stimulate aldosterone secretion Increase in Sodium
Intake- suppression of aldosterone decreases tubular reabsorption,
allowing increased Na excretion
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- Role of Aldosterone (cont.) During Chronic Oversecretion of
Aldosterone, the Kidneys Escape From Na Retention as Arterial
Pressure Rises a.Caused by tumors of the adrenal gland b.Caused by
Addisons disease
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- Nervous and Hormonal Factors (cont.) Role of ADH in Controlling
Renal Water Excretion a.Excess ADH secretion usually causes only
small increases in ECF volume but large decreases in sodium
concentration Role of Atrial Natriuretic Peptide a.Causes a small
increase in GFR and decreases in Na reabsorption
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- Integrated Responses to Changes in Na Intake High Sodium Intake
a.Activation of low pressure receptor reflexes b.Suppression of
angiotensin II formation c.Stimulation of natriuretic systems
d.Small increases in arterial pressure
- Slide 38
- Conditions That Cause Large Increases in Blood and ECF Volumes
Increased Blood Volume and ECF Volume Caused By Heart Diseases
Increased Blood Volume Caused By Increased Capacity of
Circulation
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- Conditions That Cause Large Increases ECF Volume But With
Normal Blood Volume Nephrotic Syndrome- loss of plasma proteins in
urine and sodium retention by the kidneys Liver Cirrhosis-
decreased synthesis of plasma proteins by the liver and sodium
retention by the kidneys