Peritubular Capillary Circulation
In normal man approximately 120 ml/min are filtered, but only 1 ml/min is excreted as urine. Thus over 99 percent must be reabsorbed, removed from the kidney and returned to the systemic circulation. There has been considerable recent interest in the role played by the peritubular environment, especially as it is influenced by renal haemodynamics, in the control of net reabsorption of salt and water from the proximal tubule.
The concept that has evolved reflects the possibility that changes in colloid osmotic pressure and hydrostatic pressure in tubular capillaries can influence proximal tubular reabsorption. Peritubular capillary pressure is among the lowest in the body: for example, Wunderlich and Schnermann (1969) and Falchuk and Berliner ( 1971) applied a new, remarkably sensitive pressure measuring device to assess peritubular capillary pressure in the rat kidney, and found a pressure of 65 i 0-5 mmHg, about 20-25 per cent of the value in typical systemic capillaries.
Similarly, the ultrafiltration of fluid in the glomerulus raises the colloid osmotic pressure in the peritubular capillaries: both factors favour reabsorption of water from the peritubular space. Vogel et al. (1955) provided the first experimental data suga gesting that increased colloid osmotic pressure could augment sodium transport in amphibian kidneys.
The unequivocal demonstration of active sodium transport by the proximal tubule made most investigators reluctant to accept a concept in which colloid osmotic pressure played a role. Lewy and Windhager (1968) reopened this issue when they noted a striking correlation between the filtration fraction of the kidney and the reabsorptive half-time of proximal tubular fluid and argued that both nephron load and peritubular oncotic pressure are altered by changes in the effective resistance of the efferent arterioles.
Thus, when plasma How and glomerular filtration rate did not change in parallel in the glomerulus, a force was generated which could modify fluid reabsorption downstream. Windhager (I974) has provided an excellent, concise and critical review of the experiments which have led to the conclusion that capillary colloid osmotic pressure probably influences rather than provides a primary driving force for proximal tubular fluid reabsorption.
It appears that a minimum of one-third of the tubular response to an acute reduction in glomerular filtration rate can be accounted for by this mechanism. The subsequent demonstration in the proximal tubules of amphibia that a significant fraction of ion transfer occurs via extra-cellular shunts in parallel to the transcellular path made it reasonable to assign to the space between cells a role in the osmotically induced water transfer (Windhager 1974).
According to this concept sodium is transferred from the tubular lumen to the intercellular space. A decrease in the capillary absorption could lead to a temporary pressure increase and volume expansion in the intercellular space, resulting in increased leakiness of tight junctions and thus greater backflow of Huid, and diminished net reabsorption.
A number of studies reviewed by Windhager indicate that back leak is indeed increased under conditions of reduced capillary uptake. Deen et al. (1973) and Blantz and Tucker (1975) have explored further the relationship between reabsorptive forces and peritubular plasma flow: their studies agree that peritubular capillary reabsorption is not strongly plasma How dependent~-;as opposed to glomerular filtration rate, which is highly flow dependent.
The concept that has evolved reflects the possibility that changes in colloid osmotic pressure and hydrostatic pressure in tubular capillaries can influence proximal tubular reabsorption. Peritubular capillary pressure is among the lowest in the body: for example, Wunderlich and Schnermann (1969) and Falchuk and Berliner ( 1971) applied a new, remarkably sensitive pressure measuring device to assess peritubular capillary pressure in the rat kidney, and found a pressure of 65 i 0-5 mmHg, about 20-25 per cent of the value in typical systemic capillaries.
Similarly, the ultrafiltration of fluid in the glomerulus raises the colloid osmotic pressure in the peritubular capillaries: both factors favour reabsorption of water from the peritubular space. Vogel et al. (1955) provided the first experimental data suga gesting that increased colloid osmotic pressure could augment sodium transport in amphibian kidneys.
The unequivocal demonstration of active sodium transport by the proximal tubule made most investigators reluctant to accept a concept in which colloid osmotic pressure played a role. Lewy and Windhager (1968) reopened this issue when they noted a striking correlation between the filtration fraction of the kidney and the reabsorptive half-time of proximal tubular fluid and argued that both nephron load and peritubular oncotic pressure are altered by changes in the effective resistance of the efferent arterioles.
Thus, when plasma How and glomerular filtration rate did not change in parallel in the glomerulus, a force was generated which could modify fluid reabsorption downstream. Windhager (I974) has provided an excellent, concise and critical review of the experiments which have led to the conclusion that capillary colloid osmotic pressure probably influences rather than provides a primary driving force for proximal tubular fluid reabsorption.
It appears that a minimum of one-third of the tubular response to an acute reduction in glomerular filtration rate can be accounted for by this mechanism. The subsequent demonstration in the proximal tubules of amphibia that a significant fraction of ion transfer occurs via extra-cellular shunts in parallel to the transcellular path made it reasonable to assign to the space between cells a role in the osmotically induced water transfer (Windhager 1974).
According to this concept sodium is transferred from the tubular lumen to the intercellular space. A decrease in the capillary absorption could lead to a temporary pressure increase and volume expansion in the intercellular space, resulting in increased leakiness of tight junctions and thus greater backflow of Huid, and diminished net reabsorption.
A number of studies reviewed by Windhager indicate that back leak is indeed increased under conditions of reduced capillary uptake. Deen et al. (1973) and Blantz and Tucker (1975) have explored further the relationship between reabsorptive forces and peritubular plasma flow: their studies agree that peritubular capillary reabsorption is not strongly plasma How dependent~-;as opposed to glomerular filtration rate, which is highly flow dependent.
Both physiological studies based on protein appearing in lymph draining the kidney (Pinter et al. 1974) and ultrastructural tracer studies (Venkatachalam & Karnovsky 1972) have demonstrated a highly permeable peritubular capillary system in the renal cortex. It is possible that a high interstitial protein concentration facilitates fluid flux from the intracellular space, but that is not yet clear.
Beeuwkes (1971, 1975) applied an elegant technique involving perfusion-fixation in vivo, vascular cast formation with silicone rubber and microinjection of silicone rubber of a different colour in cleared specimens to examine the relationship between vascular and tubular elements in individual nephrons. A series of complex efferent vascular patterns has emerged.
In general, the conclusion of these studies is that individual nephrons are functionally dependent on an efferent blood supply from glomeruli derived from other nephrons, and even from other zones within the kidney. Ultimately, any hypothesis concerning the peritubular control of reabsorption must be cognizant of all of these factors.
In general, the conclusion of these studies is that individual nephrons are functionally dependent on an efferent blood supply from glomeruli derived from other nephrons, and even from other zones within the kidney. Ultimately, any hypothesis concerning the peritubular control of reabsorption must be cognizant of all of these factors.