The early phase of experimental acute renal failure. III. Tubuloglomerular feedback

Abstract

Experiments were designed to determine whether tubuloglomerular feedback, which modifies nephron filtration rate in response to alterations in the macula densa sodium chloride concentration, was still apparent in the initiation phase of various types of acute renal failure. The response of the glomerulus to changes in the macula densa stimulus was evaluated in haeme pigment, ischaemic and nephrotoxic induced renal damage by measuring early proximal flow rates. The sodium chloride concentration at the macula densa was varied between low values and isotonicity in two ways: firstly, by interruption of flow through the loop of Henle, followed by orthograde perfusion with Ringer's solution; secondly, by retrograde perfusion of the loop of Henle with isosmotic mannitol or Ringer's solution. In all nephrons examined, filtration rate was inversely correlated to the macula densa sodium chloride concentration, except during orthograde perfusion with 10⁻⁴ M furosemide in Ringer's solution, when, despite the high sodium chloride concentration, filtration rate remained high. It is concluded that the mechanism of tubuloglomerular feedback is viable after the onset of compromised renal function, and may, as postulated, account for the reduction in blood flow and nephron filtration rate occurring in acute renal failure.