PDA

View Full Version : The regulation of ECF in body



Janis.Y.Chen
Fri 13th February '15, 2:03pm
ECF volume=(ECF solute content)/(ECF osmolality) nearly=(2*Na content)/(ECF osmolality)

Because the ECF osmolality is tightly controlled (constant), ECF volume varies directly with sodium content.

Generally, five aspect of factors directly affect the volume of ECF, including: 1.Renal plasma flow;2.ADH;3.Renin-angiotensin system;4.Thirst;and 5.Other factors affecting GFR.

1.Renal plasma flow

Renal plasma flow would alter GFR positively. Since the increase of renal plasma flow increase the amount of volume of plasma filtrated by glomerular in every unit of time. Besides, as the renal plasma flow increases, the rate of increase in πGC is slow down (flow-limited exchange) and the distance along the glomerular capillaries is prolonged, which makes filtrate increased and the GFR.

Factors that alter renal plasma include constriction of renal blood arterial vessels, afferent arteriolar, low effective circulatory volume etc affect GFR as described above, and stimulation of the renal nerves (sympathetic efferent fibers) also cause the vasoconstriction of renal blood arterial vessels.

2.ADH

Effective osmotic pressure of the plasma is increased above 285 mOsm/kg, the rate of discharge of neurons containing vasopressin increases and vasopressin (ADH) secretion occurs.

A decreased extracellular volume or major decrease in arterial pressure reflexively activates increased ADH secretion. To say strictly, the effective circulating blood volume affeccts ADH secretion via volume receptors. The response is mediated by neural pathways originating in cardiopulmonary baroreceptors, and if arterial pressure decreases, from arterial baroreceptors.

AngII reinforces the response to hypovolemia and hypotension by acting on the circumventricular organs to increase ADH secretion (but it is not certain which of the circumventricular organs are responsible for the increases in ADH secretion).

Some other factors such as pain, nausea, surgical stress, and emotions would affect the secretion of ADH.

Alcohol decreases ADH secretion.

3.Renin-angiotensin system

When arteriolar pressure at the level of the JG cells falls, renin secretion is enhanced.

Renin secretion is inversely proportional to the amount of Na+ and Cl- entering the distal renal tubules from the loop of Henle.

The stimulation of renal sympathetic fibers increases secretion of renin.

Besides, ang II feeds back to inhibit renin secretion by a direct action on the JG cells.

Finally, increased activity of the sympathetic nervous system increases renin secretion.

4.Thirst

Osmolality acts via osmoreceptors, receptors that sense the osmolality of the body fluids (more accurately, the plasma). These osmoreceptors are located in the anterior hypothalamus.

Decrease in ECF volume stimulate thirst by a pathway independent of that mediating thirst in response to increased plasma osmolality. Generally, the effect of ECF volume depletion on thirst is mediated in part via the rennin-angiotensin system. AngII's effects on thirst (the brain) can be antagonised by Natriuretic Hormones (ANP, BNP, CNP).

5.Other factors affecting GFR

Formula, GFR = k[(PGC – PT) – (πGC – πT)]

PGC is the mean hydrostatic pressure in the glomerular capillaries, PT is the mean hydrostatic pressure in the tubule, πGC is the oncotic pressure of the plasma in the glomerular capillaries, and πT is the oncotic pressure of the filtrate in the tubule. Normally, the πT is negligible and can be ignored. So the GFR can be calced as follows:

GFR = k[(PGC – PT) – πGC]

Changes in glomerular capillary hydrostatic pressure would affect GFR directly as explained in the formula above.

The constriction of efferent arteriolar would increase the glomerular capillary hydrostatic pressure and to maintain the GFR to some degree (When renal blood flow decreases, the constriction of efferent arteriolar due to effect of AngII help to maintain the GFR).

ANP and BNP in the circulation act on the kidneys to increase fluid and Na+ excretion and injected CNP has a similar effect. ANP: atrial natriuretic peptide (ANP), BNP: brain natriuretic peptide, and CNP: C-type natriuretic peptide. They appears to produce this effect by dilating afferent arterioles and relaxing mesangial cells. Both of these actions increase GFR.

Changes in hydrostatic pressure in Bowman's capsule.

Changes in Kf. For example, the contraction of mesangial cells produces a decrease in Kf that is largely due to a reduction in the area available for filtration.

Changes in glomerular capillary permeability.

Changes in effective filtration surface area.

References:

1.The Regular of Extracellular Fluids – ADH Secretion and Renin-Angiotensin System Tom "Prophet" Hsiung » The Regular of Extracellular Fluids – ADH Secretion and Renin-Angiotensin System (http://www.tomhsiung.com/wordpress/2014/03/the-regular-of-extracellular-fluids-adh-secretion-and-renin-angiotensin-system/)

2.Factors That Affect GFR Tom "Prophet" Hsiung » Factors That Affect GFR (http://www.tomhsiung.com/wordpress/2014/04/factors-that-affect-gfr/)

admin
Sat 21st March '15, 6:20pm
Primarily factors affecting sodium excretion

1.Sympathetic input induced reduced renal blood flow and GFR - decrease the sodium excretion.
2.Sympathetic input induced binding of alpha receptors on proximal tube - decrease the sodium excretion.
3.Sysmpathtic input induced renin secretion - decrease the sodium excretion.
4.Afferent arteriole pressure induced renin secretion - decrease the sodium excretion.
5.TG feedback induced renin secretion - decrease the sodium excretion.
6.AngII induced reduced renal blood flow and GFR - decrease the sodium excretion.
7.AngII induced increased sodium reabsorption in both proximal and distal nephron.
8.AngII induced increased salt appetite and thirst.
9.Dopamin induced decreased sodium reabsorption.

ECF volume=(ECF solute content)/(ECF osmolality) nearly=(2*Na content)/(ECF osmolality)

Because the ECF osmolality is tightly controlled (constant), ECF volume varies directly with sodium content.