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Guyton and Hall, Textbook of Medical Physiology, 12th edition
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
Fig. 29.1 Normal potassium intake, distribution of potassium in the body fluids, and potassium output from the body
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 deficiency (diabetes) Aldosterone deficiency (Addisons) Beta-adrenergic blockade Acidosis Cell lysis Strenuous exercise
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
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
PTH regulates through 3 main effects a. Stimulating bone resorption b. Stimulate activation of vitamin D which increases intestinal reabsorption of calcium
Fig. 29.11 Compensatory responses to decreased plasma ionized calcium concentration mediated by parathyroid hormone (PTH) and vitamin D
Proximal Tubular Calcium Reabsorption a. Most occurs through the paracellular pathway dissolved in water
Fig. 29.12 Mechanisms of calcium reabsorption by paracellular and transcellular pathways in the proximal tubular cells
Control of Calcium Excretion By the Kidneys Factors That Regulate Tubular Calcium Reabsorption
Decreased Ca Excretion
Increased Parathyroid hormone Decreased ECF volume Decreased blood pressure Increased plasma phosphate Metabolic acidosis Vitamin D3
Increased Ca Excretion
Decreased Parathyroid hormone Increased ECF volume Increased blood pressure Decreased plasma phosphate Metabolic alkalosis
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 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
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
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)
Regulation of Sodium Pressure Natriuresis and Diuresiskey 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
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
Distribution of ECF
Distribution of ECF Principal Factors That Can Cause Accumulation of Fluid in Interstitial Spaces a. Increased capillary hydorstatic pressure
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
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 IIdoes not usually cause large increases in ECF volume Increased Arterial Pressure Counterbalances Angiotensin II Mediated Sodium Retention
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
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
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
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
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