The excretion of sodium by the kidney is influenced by changes in glomerular filtration rate (GFR), serum sodium concentration, adrenocortical activity, the quantity of nonreabsorbable solutes in the glomerular filtrate, and the volume of extracellular fluid (ECF) (1-4). Some of these factors alter sodium excretion by affecting the amount of sodium filtered; others modulate the tubular reabsorption of sodium.The mechanism whereby acute changes in the volume of ECF influence sodium excretion is not entirely clear. At least two factors, however, have been identified. Both the secretory rate of aldosterone and the GFR are influenced by alteration in the volume of ECF and may play important roles in the regulation of sodium excretion by volume. Alteration of sodium excretion by patients with Addison's disease in a parallel fashion with sodium intake and without detectable changes in GFR (5, 6) suggests that a third factor may be operative. Furthermore, a number of investigators (7-9) have shown that, under conditions where the volume of ECF was acutely altered in the face of fixed adrenocortical activity, sodium excretion varied independently of GFR, suggesting that changes in volume were in some manner influencing the tubular reabsorption of sodium independent of adrenocortical hormones.* Submitted for publication August 7, 1963; accepted October 31, 1963. This work was supported in part by U. S. Public Health Service grants HTS-5469 and 2A-5038. All, these studies, however, are open to the objection that errors in the measurements of GFR could lead to erroneous conclusions concerning the relative roles of filtration and tubular reabsorption (1, 10).Recently, de Wardener, Mills, Clapham, and Hayter (11) circumvented this difficulty by demonstrating that acute expansion of ECF volume with an infusion of isotonic saline increased sodium excretion despite both the administration of large doses of 9a-fluorohydrocortisone and marked reductions in GFR produced by aortic constriction. These results, which have subsequently been confirmed and extended by Levinsky and Lalone (12), establish that the increased sodium excretion after expansion of the ECF volume is the consequence of diminished tubular reabsorption of sodium via some mechanism other than suppression of adrenocortical activity. They do not, however, define the locus in the nephron wherein sodium reabsorption must have been suppressed.Our experiments were designed to localize within the nephron the site at which changes in ECF volume regulate sodium reabsorption. This we achieved by demonstrating that massive infusions of hypotonic saline increase sodium excretion under the following circumstances: 1) marked reduction in GFR produced by constriction of the aorta, 2) constant and maximal aldosterone activity achieved by injections of the hormone, and 3) maximal water diuresis. Under these conditions of maximal suppression of antidiuretic hormone (ADH), the amount of filtrate delivered to the diluting segment of the nephron can be roughly approximated from the ...

Glomerular filtration rate and renal blood flow were increased in dogs by infusion of 2% glycine and hypertonic NaCl at rates of 8 ml/min. This procedure resulted both in an increased rate of sodium reabsorption and in increased oxygen consumption. Approximately six equivalents of sodium were transported per equivalent oxygen consumed, a ratio similar to that obtained by others when glomerular filtration rate had been reduced. These observations strongly suggest that a large part of renal oxygen consumption is related to the transport of sodium. When the rate of sodium reabsorption was reduced during mannitol diuresis, arteriovenous oxygen difference decreased, but renal oxygen consumption remained unchanged. It is suggested that the active sodium transport in the proximal tubules continues at an unchanged rate during mannitol diuresis but that net reabsorption is reduced owing to increased passive influx into the tubular lumen when the transtubular concentration gradient increases. Other interpretations are discussed.

Diameters of the exposed femoral artery of anesthetized dogs were continuously measured with ultrasonic elements of lead zirconate titanate. In 13 of 16 dogs vascular diameters increased following a sudden increment in arterial blood flow induced by the injection of vasodilat i ng agents (acetylcholine, histamine) peripheral to the recording level, by opening an arteriovenous shunt, or after tetanic stimulation of die sciatic nerve. The dilatation response occurred despite slight reductions in femoral blood pressure, and was present after ganglionic blockade, blockade of alpha and beta receptors with phenoxybenzamine and propranolol, atropinization and injection of an antihistamine. The dilatation response was also observed after transsection of the femoral artery distal to the recording level and is therefore not dependent on the retrograde propagation of nervous or myogenous impulses along the vascular wall. ADDITIONAL KEY WORDSarterial diameter arterial smooth muscle arteries autorcgulation blood circulation blood pressure ultrasonic vasodilator agents vasomotor system• A conduit vessel, such as the femoral artery, varies in diameter with blood pressure (1). If this were the only mode of regulation, an increase in blood flow induced by arteriolar dilatation would result in an increased pressure drop along the artery. As a consequence of the reduction in arterial blood pressure towards the periphery, the vascular diameter of the conduit vessel would decrease. However, several previous investigators (2-4), using plethysmographic methods, have found that increased blood flow was associated with an increase in the cross section of the femoral artery. Similar dilatation responses were obtained whether femoral blood flow was raised by stimulation of the sciatic nerve, injection of acetylcholine or injection of other