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

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

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

Insulin deficiency (diabetes) Aldosterone Table. 29.1 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

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

Overview of Renal Potassium Excretion Fig. 29.2

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

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

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

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

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

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

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

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

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

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

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

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

Control of Calcium Excretion By the Kidneys Fig. 29.12 Mechanisms of calcium reabsorption by paracellular and transcellular pathways in the proximal tubular cells

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

Control of Calcium Excretion By the Kidneys Factors That Regulate Tubular Calcium Reabsorption Table. 29.2 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

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

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

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

Importance of Pressure Natriuresis and Pressure 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)

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. 29.14

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

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 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

Distribution of ECF Fig. 29.16 Approximate relation between ECF and blood volume

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

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

Importance of Changes in Angiotensin II in Altering Pressure Natriuresis Fig. 29.17 Effects of excessive angiotensin II formation and blocking angiotensin II formation on the renal pressure natriuresis curve

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

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

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

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

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

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

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