1. Unit Five: The Body Fluids and Kidneys
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, 12th edition

2. Regulation of ECF Potassium Concentration and Excretion
Regulation of Internal K Distribution
Insulin stimulates K uptake into cells
Aldosterone increases K uptake into cells
Beta-adrenergic stimulation increases cellular
uptake
Acid-base abnormalities changes distribution
Cell lysis causes increased extracellular K concentration
Strenuous exercise causes hyperkalemia by releasing
K from skeletal muscles
Increased ECF osmolarity causes redistribution of K
from cells to the ECF

3. Fig. 29.1 Normal potassium intake, distribution of potassium in the body fluids, and potassium
output from the body

4. Insulin deficiency (diabetes) Aldosterone
Table Factors that can alter potassium distribution between the
intracellular and extracellular fluids
Factors That Shift K into Cells and
Decrease Extracellular K Concentration
Factors That Shift K out of Cells
and Increase Cellular K Concentration
Insulin
Insulin deficiency (diabetes)
Aldosterone
Aldosterone deficiency (Addison’s)
Beta-adrenergic stimulation
Beta-adrenergic blockade
Alkalosis
Acidosis
Cell lysis
Strenuous exercise
Increased ECF osmolarity

5. Overview of Renal Potassium Excretion
Renal Potassium Excretion- determined by
the sum of three processes
The rate of K filtration (GFR X plasma K conc.
The rate of K reabsorption by the tubules
The rate of K secretion by the tubules

6. Overview of Renal Potassium Excretion
Fig. 29.2

7. Overview of Renal Potassium Excretion (cont.)
K Secretion by Principal Cells of Late Distal and
Cortical Collecting Tubules
Fig. 29.3

8. Summary of Factors That Regulate Potassium
Increased ECF Potassium Concentration Stimulates
Potassium Secretion
Fig. 29.4

9. Summary of Factors That Regulate Potassium
Aldosterone Stimulates Potassium Secretion
Increased Extracellular Potassium Ion Concentration
Stimulates Aldosterone Secretion
Fig. 29.5

10. Fig. 29.6 Basic feedback mechanism for control of ECF potassium concentration by aldosterone

11. Fig. 29.7 Primary mechanisms by which high potassium intake raises potassium excretion

12. Summary of Potassium Regulation (cont.)
Blockade of Aldosterone Feedback System Impairs
Control of Potassium Concentration
Fig. 29.8

13. Summary of Potassium Regulation (cont.)
Increased Distal Tubular Flow Rate Stimulates Potassium
Secretion
Fig. 29.9

14. Fig. 29.10 Effect of high sodium intake on renal excretion of potassium

15. 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 body’s calcium is stored in bone
Bone, therefore, is the primary reservoir of calcium
PTH is one of the most important regulators of
calcium release

16. Control of Renal Calcium Excretion and Extracellular Calcium Ion Concentration
PTH regulates through 3 main effects
Stimulating bone resorption
Stimulate activation of vitamin D which increases
intestinal reabsorption of calcium
c. Directly increasing renal tubular calcium reabsorption

17. Control of Renal Calcium Excretion and Extracellular Calcium Ion Concentration
Fig Compensatory responses to decreased plasma ionized calcium concentration
mediated by parathyroid hormone (PTH) and vitamin D

18. Control of Calcium Excretion By the Kidneys
Proximal Tubular Calcium Reabsorption
Most occurs through the paracellular pathway
dissolved in water
b. 20% occurs through a transcellular pathway

19. Control of Calcium Excretion By the Kidneys
Fig Mechanisms of calcium reabsorption by paracellular and
transcellular pathways in the proximal tubular cells

20. Control of Calcium Excretion By the Kidneys
Loop of Henle and Distal Tubule Calcium Reabsorption
Restricted to the thick ascending limb of the Loop
Almost entirely by active transport in the distal tubule

21. Control of Calcium Excretion By the Kidneys
Factors That Regulate Tubular Calcium Reabsorption
Table Factors that alter renal calcium excretion
Decreased Ca Excretion
Increased Ca Excretion
Increased Parathyroid hormone
Decreased Parathyroid hormone
Decreased ECF volume
Increased ECF volume
Decreased blood pressure
Increased blood pressure
Increased plasma phosphate
Decreased plasma phosphate
Metabolic acidosis
Metabolic alkalosis
Vitamin D3

22. 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

23. Regulation of Renal Magnesium
More than 50% of the body’s Mg is stored in bones
Primary reabsorption site is the loop of Henle
Following lead to increased Mg excretion:
Increased ECF Mg concentration
ECF expansion
Increased ECF Ca concentration

24. 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

25. Importance of Pressure Natriuresis and Pressure
Regulation of Sodium
Importance of Pressure Natriuresis and Pressure
Diuresis in Maintaining Body Na and Fluid
Balance
Fig Acute and chronic effects of arterial pressure on sodium output
by the kidneys (pressure natriuresis)

26. Pressure Natriuresis and Diuresis—key components
Regulation of Sodium
Pressure Natriuresis and Diuresis—key components
of feedback mechanism for regulating body fluid
volumes and arterial pressure
Fig

27. Fig. 29.15 Approximate effect of changes in daily fluid intake on blood volume

28. Precision of Blood Volume and ECF Volume Regulation
Blood volume remains almost exactly constant
despite extreme changes in daily fluid intake
(Fig ); the reason is
A slight change in blood volume causes a marked
change in cardiac output
A slight change in CO causes a large change in
blood pressure
A slight change in BP causes a large change in
urine output

29. Distribution of ECF
Fig Approximate relation between ECF and blood volume

30. Distribution of ECF
Principal Factors That Can Cause Accumulation
of Fluid in Interstitial Spaces
Increased capillary hydorstatic pressure
Decreased plasma colloid osmotic pressure
Increased permeability of the capillaries
Obstruction of lymphatic vessels

31. 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
When Na intake is elevated above normal, renin
secretion is decreased, causing decreased
angiotensin II formation
When Na intake is reduced below normal, increased
angiotensin II causes Na and water retention

32. Importance of Changes in Angiotensin II in Altering Pressure Natriuresis
Fig Effects of excessive angiotensin II formation and blocking angiotensin II formation
on the renal pressure natriuresis curve

33. Angiotensin II (cont.)
Excessive Angiotensin II—does not usually
cause large increases in ECF volume
Increased Arterial Pressure Counterbalances
Angiotensin II Mediated Sodium Retention

34. 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

35. Role of Aldosterone (cont.)
During Chronic Oversecretion of Aldosterone, the
Kidneys Escape From Na Retention as Arterial
Pressure Rises
Caused by tumors of the adrenal gland
Caused by Addison’s disease

36. Nervous and Hormonal Factors (cont.)
Role of ADH in Controlling Renal Water Excretion
Excess ADH secretion usually causes only small
increases in ECF volume but large decreases
in sodium concentration
Role of Atrial Natriuretic Peptide
Causes a small increase in GFR and decreases in
Na reabsorption

37. Integrated Responses to Changes in Na Intake
High Sodium Intake
Activation of low pressure receptor reflexes
Suppression of angiotensin II formation
Stimulation of natriuretic systems
Small increases in arterial pressure

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

39. 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