TY - JOUR
T1 - Renal mechanism of action of rat atrial natriuretic factor
AU - Huang, C. L.
AU - Lewicki, J.
AU - Johnson, L. K.
AU - Cogan, M. G.
PY - 1985
Y1 - 1985
N2 - There has been conflict as to whether crude extracts of atrial natriuretic factor increase renal solute excretion by a hemodynamic mechanism or by direct inhibition of tubular transport. To investigate this issue, 7 rats were studied during a euvolemic control period and following continuous administration of pure, synthetic 24 amino acid atrial natriuretic factor. A 10- to 25-fold increase in urinary sodium and chloride excretion occurred with a brisk kaliuresis but little bicarbonaturia. Atrial natriuretic factor caused whole kidney glomerular filtration rate to increase from 1.17±0.04 to 1.52±0.07 ml/min (P < 0.005). A parallel increase in single nephron glomerular filtration rate, from 34±1 to 44±2 nl/min (P < 0.001), and from 26±1 to 37±2 nl/min (P < 0.005) was measured at the end-proximal and early distal nephron sites, respectively. Appropriate for the higher flows were an increase in absolute proximal and loop reabsorptive rates for bicarbonate, chloride, and water, with a slight decrease in fractional solute and volume reabsorption in proximal and loop segments. To exclude the possibility that atrial natriuretic factor increased filtration rate only in anesthetized animals, 8 unanesthetized rats were studied. Glomerular filtration rate increased by 45%, from 2.04±0.17 to 2.97±0.27 ml/min (P < 0.005) without significant change in renal plasma flow, as reflected by 14C-para-aminohippurate clearance (5.4±0.5-5.6±0.9 ml/min). The clearance and micropuncture data did not preclude changes in relative blood flow distribution to or in transport by deep nephron segments. In conclusion, atrial natriuretic factor appears to increase renal solute excretion predominantly by a hemodynamic mechanism without directly inhibiting superficial tubular transport.
AB - There has been conflict as to whether crude extracts of atrial natriuretic factor increase renal solute excretion by a hemodynamic mechanism or by direct inhibition of tubular transport. To investigate this issue, 7 rats were studied during a euvolemic control period and following continuous administration of pure, synthetic 24 amino acid atrial natriuretic factor. A 10- to 25-fold increase in urinary sodium and chloride excretion occurred with a brisk kaliuresis but little bicarbonaturia. Atrial natriuretic factor caused whole kidney glomerular filtration rate to increase from 1.17±0.04 to 1.52±0.07 ml/min (P < 0.005). A parallel increase in single nephron glomerular filtration rate, from 34±1 to 44±2 nl/min (P < 0.001), and from 26±1 to 37±2 nl/min (P < 0.005) was measured at the end-proximal and early distal nephron sites, respectively. Appropriate for the higher flows were an increase in absolute proximal and loop reabsorptive rates for bicarbonate, chloride, and water, with a slight decrease in fractional solute and volume reabsorption in proximal and loop segments. To exclude the possibility that atrial natriuretic factor increased filtration rate only in anesthetized animals, 8 unanesthetized rats were studied. Glomerular filtration rate increased by 45%, from 2.04±0.17 to 2.97±0.27 ml/min (P < 0.005) without significant change in renal plasma flow, as reflected by 14C-para-aminohippurate clearance (5.4±0.5-5.6±0.9 ml/min). The clearance and micropuncture data did not preclude changes in relative blood flow distribution to or in transport by deep nephron segments. In conclusion, atrial natriuretic factor appears to increase renal solute excretion predominantly by a hemodynamic mechanism without directly inhibiting superficial tubular transport.
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U2 - 10.1172/JCI111759
DO - 10.1172/JCI111759
M3 - Article
C2 - 3156153
AN - SCOPUS:0021953885
SN - 0021-9738
VL - 75
SP - 769
EP - 773
JO - Journal of Clinical Investigation
JF - Journal of Clinical Investigation
IS - 2
ER -