Biomedical Engineering Reference
In-Depth Information
there are no known sensors in the body for sodium concentration. Instead, sodium concen-
tration is regulated by changes in plasma volume, which will directly change the arterial
blood pressure. Baroreceptors, located in various places throughout the body, can sense
changes in blood pressure, and they have a direct effect on the kidneys as well as an indi-
rect effect on the kidneys. The direct effect of a reduction in blood pressure is that the glo-
merular filtration rate will reduce because the hydrostatic pressure balance across the
glomerular capillaries and Bowman's capsule decreases (see
Section 12.2
). The indirect
effect of a decreased arterial blood pressure on sodium excretion is via activation of a sym-
pathetic nervous signaling pathway. The renal sympathetic nerve directly innervates the
juxtaglomerular cells and causes them to increase the production and secretion of renin.
Renin enters the bloodstream and converts angiotensinogen into angiotensin I.
Angiotensinogen is produced by the liver and under normal conditions is always present
in the plasma. Angiotensin I is then converted into angiotensin II via an enzyme termed
angiotensin-converting enzyme (or ACE). Angiotensin-converting enzyme is bound to the
luminal surface of capillary endothelial cells and is always expressed. Angiotensin II has
various effects within the body, but the most important for sodium reabsorption is the
stimulation of the adrenal glands to produce and secrete aldosterone into the blood.
Aldosterone stimulates the cortical collecting duct epithelial cells to produce more sodium
channels and sodium-potassium ATPase pumps. This effectively increases the reabsorp-
tion of sodium (or more accurately, decreases the excretion of sodium). An increased
plasma volume has the opposite effect as described above, so that there is an increased
excretion of sodium.
Sodium drives the reabsorption of water within the nephron. As sodium ions begin to
move out of the nephron, the osmolarity of the solution within the nephron decreases. A
decrease in osmolarity can also be considered as an increase in water concentration. As
the solute moves out of the tubule lumen, the osmolarity of the interstitial fluid and/or
epithelial intercellular fluid increases, and this can also be considered as a decrease in the
water concentration. Therefore, there now exists a concentration gradient for water that
will cause water molecules to diffuse out of the tubule lumen into the interstitial space.
Water movement across the tubule epithelial cells occurs via bulk diffusion across the
tight junctions or through aquaporin channels on the luminal membrane. The proximal
tubule is very highly permeable to water, and large quantities of water are always reab-
sorbed within this segment of the nephron. The Loop of Henle experiences both water
reabsorption (descending limb) and water secretion (ascending limb) to maintain a coun-
tercurrent flow, which will not be discussed here. The water movement through the distal
tubule and the collecting duct is variable and is subject to physiological control. In a simi-
lar process to the regulation of sodium reabsorption, changes in the water reabsorption
rates of the collecting ducts are controlled by the blood volume. Decreases in blood vol-
ume will reduce the arterial pressure, which is again sensed by baroreceptors within the
cardiovascular system. This reduction causes an increase in the production and secretion
of vasopressin (or antidiuretic hormone). Vasopressin is released into the blood and even-
tually makes its way to the collecting ducts. Vasopressin then stimulates the production of
new aquaporin channels which are placed into the collecting duct epithelial membrane.
With a higher quantity of aquaporin channels within the collecting duct epithelial cell, per-
meability to water increases, and therefore, the reabsorption of water increases. With an
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