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Department of Physiology, University of Leeds.
1. Dogs were anaesthetized with chloralose and artificially ventilated. Localized stimulation of left atrial receptors for 23-25 min was achieved by distension of three small balloons at the pulmonary vein-atrial junctions and one in atrial appendage. Renal blood flows were measured by electromagnetic flow probes, glomerular filtration rate by creatinine clearance, urinary sodium excretion by flame photometry and solute excretion by osmometry. The mean aortic pressure was held constant at 92.2 +/- 2.4 mmHg (mean +/- S.E.M., n = 27) by means of a pressure bottle connected to the aorta and beta-adrenergic receptor activity was blocked by continuous infusion of propranolol (17 micrograms kg-1 min-1, I.V.). 2. In twelve dogs stimulation of left atrial receptors resulted in significant increases of 11.8 +/- 2.4% (P less than 0.001) in renal blood flow; 32.5 +/- 7.2% (P less than 0.001) in glomerular filtration rate; 19.5 +/- 5.0% (P less than 0.005) in filtration fraction: 36.3 +/- 9.0% (P less than 0.001) in urine flow: 32.7 +/- 9.2% (P less than 0.005) in sodium excretion: 36.6 +/- 9.9% (P less than 0.005) in osmolar excretion and a decrease of 31.3 +/- 11.2% (P less than 0.025) in free water clearance. Left atrial pressure and heart rate did not change significantly. In eight of the dogs ligation of the renal nerves resulted in similar changes in all of the renal variables; subsequent stimulation of atrial receptors did not cause significant changes in the renal variables. 3. In five additional dogs, in which heart rate and aortic pressure were allowed to change, stimulation of left atrial receptors for the same period resulted in significant increases in heart rate (4.3 +/- 0.7%. P less than 0.001) and mean aortic pressure (2.0 +/- 0.6%, P less than 0.025). Under this condition both the intact right kidneys and the denervated left kidneys showed significant responses in urine flow, sodium excretion, osmolar excretion and free water clearance. 4. The results show that the renal sympathetic nerves mediate the primary renal responses to atrial receptor stimulation, at least in the short term. The influence of any humoral factor in this reflex seems to be secondary to changes in heart rate and systemic blood pressure, possibly via arterial baroreceptors.
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