Feedback regulation of glomerular filtration rate
Wright, F.S.; Briggs, P.
American Journal of Physiology 233(1): F1-F7
1977
ISSN/ISBN: 0002-9513 PMID: 327832 Document Number: 113754
At least 1 of the intrarenal mechanisms serving to regulate glomerular filtration rate [GFR] operates at the single nephron level. The observation that increases in the flow rate of tubule fluid through the loop of Henle are associated with decreases in the rate of filtration by the glomerulus of the same nephron was made in several laboratories. In addition, measurements of glomerular capillary pressure (PGC) showed that this determinant of GFR was also reduced when loop flow rate was increased. The responses to changes in loop flow from normal rates were not symmetrical. Decreases in single nephron glomerular filtration rate (SNGFR) and PGC in response to increased loop flow were larger than increases in SNGFR and PGC in response to reductions in loop flow. The magnitude of the response to a given change in loop flow rate was variable: acute and chronic extracellular volume expansion decreased the response and dietary salt depletion and hemorrhage increased the response. The signal that elicits the feedback response appeared to be a correlate of loop flow. The reabsorptive transport of chloride is probably the initial step in the tranfer of information from a distal site (possibly the macula densa) to the glomerular arterioles. The final effector mechanism may predominantly involve constriction and dilation of the afferent arteriole. However, other vascular effects are possible. The mediating steps between tubule chloride transport and vasoconstriction are less certain. The renin-angiotensin system was proposed, but other locally produced factors could be involved. The functional role of the feedback mechanism is not certain. It may contribute either to autoregulation of blood flow and GFR or to homeostatic adjustments in salt and water excretion.