BASIC RENAL PHYSIOLOGY
Electrolyte and Body Fluid Regulation

ELECTROLYTE AND BODY FLUID REGULATION

A. Fluid Compartments (total about 60% of body mass)

1. Intracellular (about 36% of body mass)

a. fluid inside of cells
b. high in K+, low in Na+ and Cl-

2. Extracellular (about 24% of body mass)

a. fluid outside of cells: interstitial (between cells), blood plasma, secretions

Note: blood = plasma + cells and is about 7-8% of body mass; plasma is about 55% of blood, cells about 45%, measured by hematocrit = cell volume as a fraction of blood volume

b. high in Na+ and Cl-, low in K+

B. Fluid Movement

1. Most cells are very permeable to water
2. Extracellular fluid volume is determined by Na+; water “follows” sodium
3. Movement between intracellular and extracellular fluid is determined by osmolar concentration

C. Renal Na+ and K+ transport

1. Glomerulus: Na+ and K+ are swept into Bowman’s space by the ultrafiltration of plasma

2. Proximal tubule: Na+ is reabsorbed by active transport; K+ is reabsorbed mainly because of the concentration gradient produced by the reabsorption of water. About 70% of the Na+ and K+ entering the proximal tubule are reabsorbed

3. Loop of Henle: Na+ and K+ are reabsorbed in the ascending thick limb by active transport; about 70% of the Na+ and K+ entering the Loop of Henle is reabsorbed by the time the tubular fluid reaches the later distal tubule

4. Collecting ducts: Na+ is reabsorbed from the lumen and K+ is secreted into the lumen by active transport; the rate of transport is controlled by the renin-angiotensin-aldosterone system (major influence) and by atrial natriuretic peptide hormone

5. Excretion: Na+ and K+ remaining when fluid exits the collecting ducts is excreted in the urine

 

B. Renin

1. Synthesized by and released from the juxtaglomerular cells (modified smooth muscle cells) of the renal juxtaglomerular apparatus

2. Release controlled by

a. renal arterial/arteriolar hydrostatic pressure: P decrease => renin release; mechanism: decreased stretch of afferent arteriole granular cells
b. renal sodium at the macula densa: Na+ decrease => renin release
c. renal sympathetic activation => renin release; mechanisms:

1)fall in “central venous pressure”, as mediated by the low-pressure (atrial and venous) baroreceptors; very sensitive
2) decrease in systemic arterial pressure; mediated by carotid and aortic baroreceptors; less sensitive

3. Action: conversion of Angiotensinogen to Angiotensin I


C. Angiotensin

1. Originates from an inactive precursor -- Angiotensinogen -- produced in the liver and circulating in the blood

2. In the presence of Renin, Angiotensinogen is converted to Angiotensin I (AI); Angiotensin I is essentially biologically inactive

3. Angiotensin I is converted to Angiotensin II (AII) in the presence of Angiotensin Converting Enzyme (ACE), an enzyme which is present in the capillary endothelium, especially in the pulmonary circulation

4. actions of Angiotensin II

a. causes release of Aldosterone from the adrenal cortex
b. at high concentrations, can cause general vasoconstriction, leading to increased systemic arterial blood pressure (can cause to systemic hypertension)
c. increases proximal tubule Na+-H+ antiport and Na+-linked HCO3 reabsorption (accounts for alkalosis often seen in volume depletion)
d. contributes to thirst sensation

D. Aldosterone

1. Synthesized by and released from the adrenal cortex
2. Release stimulated by

a. Angiotensin II
b. plasma potassium: K+ increase => aldosterone release (local adrenal effect)

3. Action: increase active transport of Na-K-ATPase pump, particularly at the distal tubule and collecting duct (where it binds to a corticoid receptor in principal cells), leading to increased Na reabsorption and K excretion by the kidney (also capable of stimulating Na-K-ATPase transport in some other tissues)

E. Atrial Natriuretic Peptide (ANP)

1. Synthesis: synthesized by and released from atrial myocardial cells
2. Actions: increase renal Na excretion by

a. inhibits Na active transport in the kidney
b. inhibits renin and aldosterone secretion

3.. Control: released by atrial stretch, when atrial (or "central venous pressure") increases

F. Summary of Control