A natriuretic factor is released by saline infusion into rat renal artery.
Saline (154 mM NaCl) infused into one renal artery of anesthetized rats produced a prompt and substantial increase in sodium excretion without significant alteration of arterial pressure, renal blood flow, or glomerular filtration rate. A 1-h infusion at rates of 0.0375, 0.05, or 0.1 ml/min increased sodium excretion by the infused kidney from 0.15 +/- 0.04 to 0.70 +/- 0.12, from 0.45 +/- 0.10 to 2.17 +/- 0.40, and from 0.27 +/- 0.06 to 4.29 +/- 0.80 mumol/min, respectively. Natriuresis also occurred in the contralateral kidney. No comparable responses resulted from infusions at 0.0375 ml/min into the jugular vein, inferior vena cava, or carotid artery. Cross-circulation of blood from infused rats increased sodium excretion in uninfused recipients from 0.36 +/- 0.11 to 1.43 +/- 0.43 mumol.min-1.kidney-1. Isovolemic exchange-transfusion of blood from infused donor rats increased sodium excretion in uninfused recipients from 0.30 +/- 0.05 to 0.51 +/- 0.09 mumol.min-1.kidney-1. In both experiments, aortic infusions below the renal artery produced no comparable effect in recipient rats. Infusion of 300 mM glucose was not natriuretic. Infusion of two NaCl loads, 5.8 and 15.4 mumol/min, each at two different rates, increased sodium excretion in proportion to the load of NaCl and not to the rate of infusion. Infusions of a protein-free artificial rat plasma or of 140 mM NaCl, both with the sodium concentration of rat plasma, produced very little increase in sodium excretion. Infusion of 154 mM sodium lactate produced an increase in sodium excretion comparable to that produced by 154 mM NaCl. Reducing the infusion rate of 154 mM NaCl from 0.05 to 0.01 ml/min produced a rapid decline in the rate of sodium excretion. We conclude that renal arterial saline infusion activates a mechanism that increases sodium excretion by the infused kidney and concurrently causes the release of a natriuretic factor. Increased sodium concentration in renal arterial blood was the only stimulus found to produce the effect.
Bullivant
E M
EM
Department of Physiology, School of Medicine, University of Auckland, New Zealand.
Muñoz
D J
DJ
D000818:Animals; D003427:Cross Circulation; D005078:Exchange Transfusion, Whole Blood; D007262:Infusions, Intravenous; D007269:Injections, Intra-Arterial; D007668:Kidney / Q000187:drug effects; D008297:Male; D009318:Natriuresis / Q000187:drug effects; D045283:Natriuretic Agents / Q000378:metabolism*; D010952:Plasma Substitutes / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D012039:Regional Blood Flow; D012077:Renal Artery / Q000502:physiology*; D012965:Sodium Chloride / Q000494:pharmacology*
D045283:Natriuretic Agents; D010952:Plasma Substitutes; D012965:Sodium Chloride