A Current Concept of the Regulation of Blood Volume

Abstract

To the unspecialized reader concerned with management of the aedema of disease, the rapid accumulation of proven influences on the renal regulation of extracellular electrolyte content and fluid volume may pose a problem in integration. This presentation does not constitute a comprehensive review (Smith, 1957;Grossman, 1957) but rather a summary of present understanding of a homeostatic mechanism, the existence of which is receiving tentative acceptance. This mechanism appears to operate primarily by correcting variations in the content of the intravascular compartment of extracellular fluid volume. Secondary changes in the same direction will normally occur almost concomitantly in the interstitial fluid compartment, which must be thought of as essentially continuous with the intravascular space. Exchange and distribution of fluid between these two compartments are chiefly determined by hydrostatic and colloid osmotic pressure differences and by capillary permeability. The latter factors may be grossly altered by disease but can play no active role in governing the overall volume of extracellular fluid in the normal state.The work of Verney (1947, 1957) has already established the features of another mechanism evolved to maintain the constancy of osmotic pressure of body fluid. One may now visualize the sequence of events following water loading as a reduction in plasma osmotic pressure causing osmoreceptors in the anterior hypothalamus to reduce the secretion ofantidiuretichormone via the posterior pituitary gland, thus leading to a reduced renal tubular reabsorption of water and a consequent diuresis. This renal response corrects both the reduced osmotic pressure and the increased volume.The opposite situation, ingestion of a strongly hypertonic solution, leads to a retention of water by the kidney and to increased water intake which, although effective in returning osmotic pressure to normal, do so by enlarging extracellular fluid volume. This volume increase, like that produced by ingestion or infusion of isotonic solution and, on the other hand, the reduced volume following haemorrhage are, in fact, followed by other appropriate renal responses that operate to restore normal volume. For some years the acceptance of a classical reflex mechanism to regulate blood volume has been delayed by refuge taken in the simpler view that increased blood volume must lead to increased renal blood flow and hence to greater renal output. An automatic regulating device is thus provided. The evidence is commonplace, however, that glomerular filtration rate does not necessarily vary with renal blood flow or with blood pressure. Even admitting the probability that tubular reabsorption may be influenced by renal hemodynamic changes affecting the concentrating mechanism (Goodyear et al., 1958; Gottschalk and Mylle, 1959), the evidence that extrarenal factors are involved is now overwhelming. A logical approach to the understanding of a reflex mechanism for regulating blood volume would be a search for the classical components, a...

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