Volume budget

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All control loops of an organism that serve to keep the volume of the body water constant ( homeostasis ) are summarized under volume balance . Contrary to what one would intuitively assume, the volume regulation does not primarily consist in the regulation of the water, but in the regulation of the salts; the water follows these within the framework of osmoregulation . In the narrower sense of the word, “volume” refers to the water outside the cells ; Volume deficiency ( hypohydration , symptom: circulatory weakness) and excess volume ( hyperhydration , symptom: high blood pressure, edema) are of great practical medical importance here.

Salt and liquid distribution

The distribution of body water can be simplified as follows: 60% of the body weight of an adult consists of water . ⅔ of which are in the intracellular space , ⅓ in the extracellular space . Most of the extracellular water is in the interstitial fluid, around etwa is blood plasma , and an even smaller part is transcellular fluid. The plasma makes up about 55% (1 minus hematocrit ) of the blood, the rest are cellular components, primarily erythrocytes .

Water can move freely throughout the body. Driven by the osmotic pressure, it compensates for all differences in osmolarity , so that the same osmolarity of around 300 mosmol / l occurs everywhere in the body (except in the renal medulla ). Osmoregulation therefore takes place by controlling the supply and excretion of water.

In contrast, salts can only cross cell membranes in a strictly regulated manner. Sodium is mainly located extracellularly due to the work of the sodium-potassium pump , while potassium is concentrated intracellularly. As long as the amount of salt in the compartments is normal, the volume ratio intracellular / extracellular always remains 2∶1. Since missing or superfluous water only ever affects a third of the extracellular space, only pronounced osmotic disorders can cause classic volume problems. In contrast, with intact osmoregulation, sodium deficiency or excess manifests itself as an isolated reduction or enlargement of the extracellular space.

Regulation of the extracellular fluid volume

Since the blood plasma is part of the extracellular space, a reduced extracellular volume is also expressed in a reduced blood volume and thus in a reduced central venous pressure . Via the Frank-Starling mechanism , a lower central venous pressure also leads to a lower arterial blood pressure. Long-term blood pressure regulation is therefore volume regulation.

The decisive control circuits of volume homeostasis belong to the renin-angiotensin-aldosterone system : The liver synthesizes the plasma protein angiotensinogen ; The enzyme renin , which is released into the bloodstream by the juxtaglomerular cells of the kidney when there is insufficient volume , splits angiotensin I off from it. This results in a further cleavage that is catalyzed by the membrane-based angiotensin-converting enzyme (mainly in the pulmonary vessels), angiotensin II . Angiotensin II in turn promotes the formation and release of aldosterone in the zona glomerulosa of the adrenal cortex . The effects on the sodium balance, through which the volume increases and the control loop is finally closed with negative feedback , are based on angiotensin II and aldosterone; Angiotensin II also has a vasoconstricting effect and is therefore also part of short-term blood pressure regulation .

Natriuretic peptides ( ANP , BNP , CNP ) have stimuli and effects opposite to the renin-angiotensin-aldosterone system and are more of pathophysiological importance.

Sensors

The juxtaglomerular cells are sympathetically ( noradrenergic ) innervated modified smooth muscle cells . Locally measured low blood pressure directly increases renin release. Sympathetic stimulation increases when the stretch sensors in the atria of the heart and the baroreceptors in the aorta and carotid are inactive; also circulating adrenaline , which is released in the adrenal medulla (also sympathetically), promotes the release of renin. The formation of aldosterone is not only determined by angiotensin II, but also directly stimulated by low sodium and high potassium concentrations.

Actuators

Angiotensin II stimulates the reabsorption of sodium in the proximal tubule, in the central nervous system it causes thirst and an appetite for salt. Aldosterone stimulates sodium reabsorption in the collecting tube (distal tubule), sodium absorption in the intestine and sodium reabsorption in the excretory ducts of the sweat glands.

Low central venous pressure (measured by the atrial strain sensors) and angiotensin II stimulate the release of ADH, the central hormone of osmoregulation. It does not have to come to hyperosmolarity first, so that an increase in the sodium level for the purpose of increasing the volume is followed by the necessary water.

Disruptions 

Normal      ■ez■|■■■iz■■■

           Hypohydratation
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hyperton    □■■■|■■■■■■□□

           Hyperhydratation
hypoton    ▦■■■■|■■■■■■■■▦▦
isoton     ▦■■■■|■■■■■■■■
hyperton  ▦▦■■■■|■■■■■■□□
  • To prevent swelling or shrinkage of cells, osmohomeostasis usually takes precedence over volume homeostasis. Since the extracellular osmolarity is largely determined by the sodium concentration, a deficiency / excess of sodium leads to isotonic hypo- / hyperhydration.
  • Only in the event of pathological changes in volume does the body accept deviations from normal osmolarity so that the volume deviation is lower. The hypotonic hypohydration / hypertonic hyperhydration that occurs with pronounced sodium deficiency / excess can in this respect be viewed as a superimposition of a volume disorder with a compensatory counter-rotating osmolarity disorder. This makes it understandable that the intracellular volume is increased in hypotonic hypohydration and decreased in hypertonic hyperhydration.
  • These volume disorders should be distinguished from hypertonic hypohydration and hypotonic hyperhydration, which represent osmotic disorders as a lack / excess of pure water .

Sodium losses can occur renally ( kidney failure , aldosterone deficiency in the case of adrenal insufficiency , iatrogenic through diuretics ) or extrarenally (diarrhea, vomiting, fistulas). The resulting real volume deficiency is treated by giving full electrolyte solutions; Pretzel sticks and cola as home remedies for diarrhea can also be seen in this context. An increased sodium level is found in hyperaldosteronism , heart failure and extracellular edema of all kinds.

Drug influence

Inhibitors of the renin-angiotensin-aldosterone system are used to treat (primary) high blood pressure : ACE inhibitors prevent the formation of angiotensin II from angiotensin I , sartans displace angiotensin II from the angiotensin II receptor of type 1. Aldosterone antagonists compete with aldosterone to bind to its intracellular receptor. By inhibiting the sympathetically stimulated renin release, beta blockers also develop part of their effect by reducing volume.

In addition, drugs are available that promote sodium excretion by directly blocking the renal transport of sodium. Important groups of active ingredients here are loop diuretics , thiazide diuretics and ENaC blockers. The particularly effective loop diuretics are often used to treat edema.

literature

  • Robert Franz Schmidt , Florian Lang, Manfred Heckmann (eds.): Physiology of humans . 31st edition. Springer Medizin Verlag, Heidelberg 2010, ISBN 978-3-642-01650-9 , Chapter 30 Water and electrolyte balance .