A CURRENT CONCEPT OF THE REGULATION OF BLOOD VOLUME

Abstract

In addition to mechanisms for the regulation of osmotic pressure of the extracellular fluid, the major factor determining intracellular volume (Robinson, 1960), a complex mechanism exists for the regulation of extracellular fluid volume. The latter mechanism appears to depend upon sensory information from volume receptors in the low pressure and high pressure sides of the circulation, and possibly also in the interstitial fluid compartment. The volume of the extracellular compartment is adjusted first by changes in circulating blood volume, brought about by alterations in urinary water and electrolyte output. The low pressure system receptors appear to regulate mainly the renal water output by varying the level of secreted antidiuretic hormone their function may be conceived as the protection of the low pressure system and heart from overloading. The high pressure system receptors appear to regulate mainly the sodium output by varying the production of aldosterone; the parameter of pulse pressure, related to stroke cardiac output, is probably the relevant stimulus to volume regulation by these receptors, the function of which may be conceived as the maintenance of adequate tissue fluid circulation. An additional regulation of urinary sodium excretion must exist, and there is evidence supporting at least 2 possible mechanisms: a natriuretic hormone, secreted in the midbrain, or renal haemodynamic control of the tubular concentrating mechanism. The coordinating centres for the homeostasis of blood volume seem to lie in the midbrain, with the anterior hypothalamic centres controlling water output and the posterior diencephalic centres, possibly including the pineal gland, controlling sodium output. The salt retention of cardiac failure can, in some cases only, be explained on the basis of reduced cardiac output leading to increased aldosterone secretion in spite of the overruled opposing influence from engorgement of the lesser circulation. An abnormally increased renal reabsorption of water and salt, due to a raised filtration fraction or an enhanced sensitivity to aldosterone, may contribute to salt and water retention in edema. Although its disorder in disease is poorly understood, the existence of a mechanism to regulate blood volume in the normal state must now be accepted among the homeostatic mechanisms designed "to maintain the constancy of the internal environment".