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The converse occurs if sodium intake falls.

In some disease states the relationship between effective circulating volume and extracellular volume breaks down. Potassium excretion and distal tubular flow Hodroelectrolitico excretion seems to be closely related to distal tubular flow, increasing with a rise in flow and decreasing as flow falls.

Because sodium is the major solute within the extracellular compartment, plasma sodium concentration is the principal osmotic factor controlling ADH secretion. Therapy with loop diuretics, by inhibition of sodium and chloride reabsorption, can therefore decrease magnesium reabsorption, resulting in magnesium depletion.


Urea is an ineffective osmole and glucose is present at a much lower concentration than sodium, except during severe hyperglycaemia. Convert documents to beautiful publications and share them worldwide.

These conditions can promote water retention at the cost of osmoregulation through the hypovolaemic stimulus to ADH as discussed above. Although plasma osmolality is determined principally by plasma sodium concentration, osmolality is regulated by changes in water balance that bring about dilution or concentration of solute.


Activation of V1a receptors also promotes release of procoagulant factors and enhances platelet adhesiveness. Renin—angiotensin system The RAS has several functions, but is principally concerned with maintenance of pressure and volume. An antidiuretic mechanism not regulated by extracellular fluid tonicity.

A solute is able to generate an osmotic pressure across a membrane only if it is unable to cross that membrane.


Volume regulation In contrast, volume regulation is brought about largely through changes in sodium excretion. Pressure natriuresis Changes in blood volume directly alter cardiac output and blood pressure. Renin secretion is also stimulated whenever effective circulating volume falls, and is suppressed when it is restored.

This is well illustrated by considering the consequences hidroeectrolitico an abrupt rise or an abrupt fall in plasma osmolality.

The results of studies of transplanted patients with renal or cardiac denervation, who are, nevertheless, able to maintain normal salt and water hirdoelectrolitico, have shown that these mechanisms are not interdependent and that no single receptor is dominant.


It is in proportion to the increase in sodium intake. It causes vasodilation and increases urinary excretion of sodium and water. Sodium is the major extracellular cation.

However, hypovolaemia can generate much higher ADH levels. Osmoreceptors and the hypothalamo-pituitary tract, which regulates secretion of anti-diuretic hormone Paraventricular neurones Third ventricle Supraoptic neurone Optic chiasm Anterior hypophyseal artery Portal venous system Anterior pituitary Posterior pituitary Systemic venous drainage Anti-diuretic hormone, synthesized in the supraoptic osmoregulatory and paraventricular volume-sensitive nuclei adjacent to the third ventricle, is transported along axons and secreted in the posterior pituitary, the portal venous system and into the cerebrospinal fluid Figure 2 Changes in plasma anti-diuretic hormone Changes in plasma anti-diuretic hormone ADH with increasing plasma osmolality a and volume depletion b.

Balance hidroelectrolítico neonantal by on Prezi

It can be seen that there is no direct relationship between plasma sodium concentration which is the principal determinant of osmolality and plasma volume. After reading this article, you should be able to: Creating downloadable prezi, be patient.


Magnesium reabsorption in the ascending limb is also inhibited by hypercalcaemia and is dependent on potassium secretion. Maintenance of plasma volume is essential for adequate tissue perfusion. ADH is produced in the supraoptic and paraventricular nuclei of the hypothalamus, and then migrates along the axons of these neurones into the posterior pituitary Figure 2. Atrial natriuretic peptide This is a polypeptide hormone consisting of 28 amino acids that is synthesized in myocardial cells by cleavage of a precursor pro-ANP.

Their homeostasis relies hidrorlectrolitico systems that regulate water balance and, as the principal extracellular solute, sodium balance. Salt loading expands the extracellular volume, decreasing renin secretion, whereas salt deprivation causes contraction of the extracellular volume, stimulating renin secretion. V1a receptors have a pressor effect on vascular smooth muscle cells, through activation of phosphoinositol.

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. The renal receptors influence the RAS directly. Unlike the other adrenal cortical hormones, aldosterone hidroelectrolitivo not regulated by adrenocorticotropic hormone, but by the RAS and also by plasma potassium. These relay through the vasomotor centre in the brainstem to the sympathetic nervous system.