The food content of sodium and urinary excretion regulate the total body amount of sodium. If the total body amount of sodium and volume of ECF are low, the kidneys increase the sodium conservation. If the total amount of sodium body and the volume of ECF are high, the excretion of sodium (natriuresis) is amplified so that the volume decreases.
Since sodium is the most important osmotically active ion of the extracellular fluid (ECF), the total amount of body determines the volume of ECF of sodium. Lack of or overload with sodium caused a lack of volume (volume deficiency) or volume overload in the ECF (volume overload). Serum sodium concentrations do not necessarily reflect the total amount of body sodium. The food content of sodium and urinary excretion regulate the total body amount of sodium. If the total body amount of sodium and volume of ECF are low, the kidneys increase the sodium conservation. If the total amount of sodium body and the volume of ECF are high, the excretion of sodium (natriuresis) is amplified so that the volume decreases. The renal sodium excretion can be adapted to a considerable extent to the sodium intake. The renal sodium excretion requires a transport of sodium in the kidneys and is thus dependent on renal blood flow and GFR. Thus, an inadequate sodium excretion in the context of a reduced renal blood flow, such. As in chronic kidney disease or heart failure occur. Renin-angiotensin-aldosterone axis, the renin-angiotensin system is the most important regulatory mechanism of renal sodium excretion. In the state of volume deficiency GFR and sodium transport to the distal nephron decrease, resulting in the release of renin. Renin cleaves angiotensinogen (renin substrate) to form angiotensin I. ACE (angiotensin converting enzyme) then cleaves angiotensin I to angiotensin II Angiotensin II has the following effect:. Increased sodium retention by lowering the filtration rate of sodium and an increase in sodium re in the proximal tubule. Elevated blood pressure (has pressor effect) Increased thirst direct impaired water excretion stimulates the adrenal cortex to secrete aldosterone, which leads via renal mechanisms to an increase in renal Na reabsorption. Angiotensin I can also be converted into angiotensin III, which stimulates aldosterone secretion to the same extent as Angiotensin II, however, has a lower vasopressor activity. The aldosterone secretion is stimulated by hyperkalemia. Other natriuretic factors more different natriuretic factors have been identified. These include atrial natriuretic peptide, cerebral (brain) natriuretic peptide (BNP) and C-type natriuretic peptide (CNP). ANP is secreted from atrial tissue of the heart. The concentration increases in volume overload of the ECF (for. Example, when heart failure, chronic kidney disease, cirrhosis with ascites), the primary aldosteronism and in some patients with a primary arterial hypertension. Decreased values ??have been observed in some patients with nephrotic syndrome and suspected decrease in volume of ECF. High concentrations increase sodium excretion and increase the GFR, even if the blood pressure is low. BNP is synthesized mainly in the atria and in the left ventricle and has similar triggers and effects such as ANP. BNP assays are available, a high BNP concentration is used to diagnose a volume overload. CNP, unlike ANP and BNP, acting vasodilator in the first place. Sodium deficiency or surplus is a sodium deficiency caused by insufficient sodium intake and increased losses through the skin, the gastrointestinal tract or kidneys (impaired renal sodium conservation). Impaired renal sodium retention may be caused by a disease of the kidney itself, adrenal insufficiency or a diuretic therapy. A sodium overload sets a higher sodium intake advance as excretion. Since healthy kidneys can excrete large amounts of sodium, a sodium overload is usually a sign of a disturbed regulation of renal blood flow and excess sodium (eg. As in heart failure, cirrhosis, chronic kidney disease).