![]() zona glomerulosa of the adrenal glands (sodium concentration, which is affected by extracellular fluid volume changes indirectly, as the result of water retention by vasopressin, the release of which is stimulated by hypotension).carotid and aortic baroreceptors (blood pressure).However, indirect mechanisms for sensing volume do exist, and they mainly depend on sensing the performance of the cardiovascular system, which is affected by extracellular volume. Decreased intravascular volume: unlike individual cells, which have cytoskeletal tension and membrane stretch-activated mechanisms to detect volume, the extracellular fluid compartment is not equipped with any sensor to help it determine how full it is.Regulation of extracellular fluid volume:.Effect: Increased aquaporin expression and increased water permeability of the cortical collecting duct cells, with the result being increased water reabsorption.Effectors: cortical collecting duct cells.Efferent: vasopressin secretion from the posterior pituitary and binding to renal V2 receptors.Afferent: fibres from nucleus of the solitary tract and from abovementioned osmoreceptors. ![]() Sensor: the subfornical organ and organum vasculosum lamina terminalis, small circumventricular organs that do not have a blood-brain barrier and are therefore sensitive to changes in tonicity (not osmolality- they seem to deprioritise ineffective osmoles).Regulation of extracellular fluid tonicity, that can also result in changes to extracellular fluid volume as a byproduct:.Where the tonicity of the extracellular fluid is low, but the volume is also low, vasopressin secretion is sustained even though it may lead to a decrease in tonicity by the retention of water.Īlternatively, in a sensor-controller-effector matrix beloved by college examiners:.Conflict between these systems is resolved in favour of volume:.RAAS-mediated changes in sodium handing by the kidney produce a reabsorption of sodium, increasing volume and inhibiting vasopressin secretion.Vasopressin-mediated retention of water to restore normal tonicity in a hypertonic state also restores volume, reducing RAAS activity.Both systems affect each other's function, and are complimentary:.The shape, size and pressure of the actual extracellular compartment is largely irrelevant, as the fluid it in is incompressible, and animal cells cannot sustain pressure gradients because they lack a cell wall.mainly regulated by neurohumoral mechanisms that control the renal handling of sodium in response to changes in the function of the circulatory system:.the function of the osmotically active content of the extracellular fluid (mainly sodium and chloride).how much of the total body water is osmotically drawn into the extracellular fluid, which is: Total body water content, which is carefully regulated mainly by vasopressin, by adjusting thirst and the renal handling of water.The volume of the extracellular fluid is mainly dependent on two factors:.So as not to reproduce content already available elsewhere in this site, the short summary offered here is linked to relevant pages. On this shaky premise, what follows will focus mainly on the defence of volume, leaving discussions of tonicity to the ridiculously apocryphal chapter dealing with the osmoregulatory role of vasopressin. In defense of this strategy, neurohormonally mediated changes in volume do not necessarily produce changes in tonicity, as the retained fluid should generally be isotonic, whereas changes in tonicity usually do produce changes in volume because they involve the manipulation of water. The problem is that most textbooks divide these into "the defence of volume" and "the defence of tonicity", as if these are somehow completely separate. The main problem of trying to write about this was that the volume of the extracellular fluid is controlled by two parallel and interdependent regulatory pathways: the regulation of body water (by vasopressin and thirst) and the regulation of osmotically active solute in the extracellular fluid (which is mainly sodium, and mainly mediated by the humoral factors like renin angiotensin aldosterone and the natriuretic peptides). Both are necessary for the maintenance of normal extracellular fluid volume and tonicity, and both respond to changes in both volume and tonicity, and also each can activate the other. The author, bound by his unexplainable attachment to the CICM syllabus document, found it rather difficult to navigate the narrow channel between "humoral regulation of blood volume" and "distribution and movement of body fluids", as both will inevitably involve some of the same physiological systems. It is also probably related to SectionG5(iv), " explain the humoral regulation of blood volume and flow". This chapter vaguely recalls Section I1(i) of the 2017 CICM Primary Syllabus (" explain the distribution and movement of body fluids").
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