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Salt loading expands the extracellular volume, decreasing renin secretion, whereas salt deprivation causes contraction of the extracellular volume, stimulating renin secretion. It is accompanied by anions, principally chloride and bicarbonate.


Both actions tend to correct hypovolaemia and hypotension, supporting tissue perfusion. Volume receptors The major volume receptors can be divided into extra-renal and intra-renal groups.

The steady state The discussions so far have dealt principally with responses of the regulatory systems for water and salt balance to acute perturbations. Most atrial natriuretic peptide ANP -producing cells are within the atria, responding to an increase in stretch. The differences between osmoregulation and volume regulation are emphasized by considering manoeuvres that would perturb the homeostasis of the three fluid compartments.

In hidroeelctrolitico disease states the relationship between effective circulating volume and extracellular volume breaks down. Clinical physiology of acid-base and electrolyte disorders, 5th edn. Thirst is also stimulated. These conditions can promote water retention at the cost of osmoregulation through the hypovolaemic stimulus to ADH as discussed above. Conditions characterized by a low effective circulating volume can lead to water retention in the face of evolving hyponatraemia, as seen in cardiac failure and hepatic cirrhosis.

Effective osmolality The osmolality of a solution is determined by the number of molecules of osmotically active hjdroelectrolitico contained in that solution. Pressure natriuresis Changes in blood volume directly alter cardiac output and blood pressure.



Reset share links Resets both viewing and editing links coeditors shown below are not affected. This is converted enzymatically to an octapeptide, angiotensin II, primarily by angiotensin-converting enzyme in the pulmonary capillaries. Sodium retention is achieved through two mechanisms: The systems regulating salt balance, and thus volume, are essentially aimed at preservation of tissue perfusion, which is sensed as the effective circulating volume see below.

Maintenance of plasma volume is essential for adequate tissue perfusion. These systems must also be able to accommodate changes in salt intake. Unlike the other adrenal cortical hormones, aldosterone is not regulated by adrenocorticotropic hormone, but by the RAS and also by plasma potassium.

This tends to oppose the actions of ADH on the principal cells of the distal nephron and might constitute a negative feedback loop. Experimental evidence indicates that ANP effects an increase in sodium and water excretion by increasing GFR and decreasing sodium absorption in both the proximal and distal nephron segments.

It is in proportion to the increase in sodium intake. Natriuretic peptides Sodium loading results in an appropriate increase in sodium excretion.


Increased water intake driven by thirst, together with water preservation driven by ADH release, returns elevated osmolality to normal or, if it is volume driven, helps to correct volume depletion. Conversely, low distal flow and less efficient clearance of secreted potassium within the lumen would be expected to produce a less favourable electrochemical gradient for continued potassium secretion.

Changes in sodium balance lead to changes in plasma volume and are sensed principally through changes in the circulation. The renal volume receptors comprise baroreceptors in the juxtaglomerular apparatus of the afferent arteriole and the macula densa in the early part of the distal tubule which sense a fall in distal delivery of sodium chloride.


It is, therefore, appropriate that thirst tends to be satisfied quickly by consumption of water but recurs in bursts. There seems to be no mechanism to protect against hypermagnesaemia, which occurs if intake is maintained in the face of declining renal function. Calculated and measured osmolality In normal circumstances, plasma osmolality can be derived from the concentrations of the three principal solutes as follows: Consider infusion of hypertonic saline.

Because sodium is the major solute within the extracellular compartment, plasma sodium concentration is the principal osmotic factor controlling ADH secretion. Potassium excretion is increased, correcting the plasma potassium concentration.

The distal nephron regulates renal potassium excretion under the control of aldosterone. The consequent changes in angiotensin II and aldosterone activity result in sodium excretion or retention respectively, correcting the extracellular volume. Control of anti-diuretic hormone release: Anti-diuretic hormone, distal flow and potassium excretion Distal potassium excretion is stimulated by ADH. Conversely, volume depletion stimulates RAS activity and aldosterone in order to increase sodium and water retention, but aldosterone-driven potassium secretion might be expected to cause potassium depletion.