The validity of the lithium clearance technique as a measure of end-proximal fluid delivery was assessed using micropuncture in sodium-replete, Inactin-anesthetized Sprague-Dawley rats. Three groups of animals were used: controls, amiloride treated, and furosemide treated. Diuretic-induced salt and water losses were replaced. Fractional lithium excretion (FELi) was 0.23 +/- 0.01, 0.24 +/- 0.02, and 0.40 +/- 0.03 in the control, amiloride, and furosemide groups, respectively. In each group, the tubular fluid-to-plasma lithium concentration ratio at the end of the proximal convoluted tubule (PCT) was significantly greater than unity (control, 1.16 +/- 0.03; amiloride, 1.16 +/- 0.02; furosemide, 1.17 +/- 0.02). In the control group, fractional lithium delivery (FDLi) at the late PCT was 0.50 +/- 0.02, while FDLi at the early distal tubule was 0.25 +/- 0.01; the latter did not differ significantly from FDLi at the late distal tubule or from FELi. Values in amiloride-treated rats were almost identical. Furosemide had no effect on FDLi at the late PCT, but raised that at the early distal tubule to 0.37 +/- 0.03. We conclude that 1) lithium reabsorption in the PCT lags slightly behind that of water, 2) substantial furosemide-sensitive lithium reabsorption occurs beyond the PCT, and 3) no significant lithium reabsorption occurs in nephron segments beyond the loop. These findings call into question the use of lithium clearance as a quantitative measure of end-proximal fluid delivery in sodium-replete animals.

SUMMARY1. The possible pressor effect of vasopressin immediately after acute haemorrhage has been studied using anaesthetized Brattleboro rats with diabetes insipidus and rats of the Long Evans parent strain.2. A blood loss of 0.5 % of the body weight caused a significant decrease in mean arterial blood pressure, measured 10 min later, in Brattleboro rats, whereas this degree of haemorrhage was non-hypotensive in the control Long Evans rats.Following subsequent blood losses (each of 0-5 % of the body weight), mean arterial blood pressure in Brattleboro rats was always significantly lower than in Long Evans rats.3. While no antidiuretic activity was at any time found in the plasma of Brattleboro rats, haemorrhages greater than 1 % of the body weight were associated with marked increases in plasma arginine vasopressin (AVP) of Long Evans rats. 4. When Brattleboro and Long Evans rats were subjected to a single haemorrhage of 2 % of the body weight, the immediate decrease in arterial blood pressure was similar in the two groups. However, 5 and 10 min after the haemorrhage the arterial blood pressure was significantly higher in the Long Evans rats. When vasopressin was infused into Brattleboro rats so that plasma levels of the hormone approached those found in Long Evans rats, the mean arterial blood pressure 0, 5 and 10 min after haemorrhage was similar to that in the Long Evans animals. 5. It is concluded that in the anaesthetized rat, vasopressin plays an important role in the regulation of arterial blood pressure during the period immediately following acute haemorrhage.

SUMMARY1. Adult rats were unilaterally nephrectomized and the weight of the remaining kidney up to 42 days after the operation compared with that of rats of comparable weight which underwent a sham operation.2. After unilateral nephrectomy the rate of renal hypertrophy varied with the protein content of the diet: it was faster when animals were fed on a high protein diet (22 % casein) and lowest in animals fed on a low protein diet (7 % casein).3. In rats fed on a standard diet (18 % casein), after unilateral nephrectomy there was a sharp increase in glomerular filtration rate (G.F.R.), as measured by inulin clearance estimations; this was accompanied by an enhanced oxygen uptake and by an increase of RNA/DNA ratios in the renal cortex. Changes in rate of oxygen uptake and of RNA/ DNA ratios in the medulla were negligible.4. A marked increase in mitotic activity of cells of the cortex occurred only 48 hr after the operation. It lasted for about 2 days. No significant changes in mitotic activity of cells in the medulla were observed. 5. After its initial marked rise glomerular filtration rate in the renoprival kidney settled down to about 30-40 % above its pre-operative level, and remained at that level for the whole period of observation (6 weeks), while the increase of oxygen uptake returned to its control level in some 10-14 days. RNA/DNA ratios in the cortex remained high, but did not increase further. 6. The increase of RNA/DNA ratios in the renal cortex was correlated with a steady increase in the dry weight of the renoprival kidney.7. Water and solutes excretion were restored to normal in about 3-5 days after the operation.8. Though the increase in glomerular filtration rate may be the prime mover in the mechanism of compensatory renal hypertrophy, it does not explain why there is an increase in the size of tubules.

SUMMARY1. The ligation of one ureter is accompanied by compensatory hypertrophy of the contralateral kidney.2. The rate of growth of the contralateral kidney after ligation of the opposite ureter is similar to that observed after unilateral nephrectomy.3. Ligation of one ureter produced ipsilateral hydronephrosis. 4. The development of hydronephrosis was accompanied by a marked increase of DNA, suggesting hyperplasia, and of the rate ofanaerobic glycolysis, while the rate of oxygen uptake decreased, especially in the cortex.5. During compensatory hypertrophy of the contralateral kidney, after ligation of the opposite ureter, there were increases of RNA/DNA ratios and of oxygen uptake, especially marked in the cortex, and in every respect similar to those observed after unilateral nephrectomy.6. Ligation of one ureter resulted in an increase of glomerular filtration rate of the contralateral kidney similar to that observed after unilateral nephrectomy.7. The mechanisms of contralateral renal hypertrophy after ligation of one ureter and after unilateral nephrectomy are discussed. It is suggested that in both cases the prime mover to compensatory hypertrophy is the increase of glomerular filtration rate.

SUMMARY1. Anaesthetized Brattleboro rats with hereditary diabetes insipidus were infused with vasopressin at three different doses (1P3, 13 or 130 mu./hr) in order to study the effect ofthe hormone on renal blood flow and its distribution. Radioactive microspheres were used to determine intrarenal blood flow. 2. The plasma vasopressin level during infusion of the lowest dose was calculated to be within the physiological range. At this dose vasopressin was antidiuretic but was without effect on arterial blood pressure or solute excretion, whereas the two higher doses were both pressor and natriuretic.3. All doses of vasopressin increased renal vascular resistance and decreased renal blood flow. The vasoconstrictor effect of the lowest dose was confined to the outer cortex, whereas the two higher doses affected the entire cortex.4. In separate experiments, [1-(,-mercapto-fl,fl-cyclopentamethylenepropionicacid), 2(0-methyl) tyrosine] arginine vasopressin, an antagonist of the vascular action of vasopressin, was administered to anaesthetized Long Evans or Brattleboro rats. In the Long Evans rats the antagonist caused a decrease in renal vascular resistance and a consequent increase in renal blood flow, this effect being restricted to the outer cortex. In Brattleboro rats the antagonist had no effect on renal vascular resistance or renal blood flow.5. It is concluded that physiological levels of vasopressin influence the distribution of renal blood flow by causing vasoconstriction in the outer region of the renal cortex. Higher levels of the hormone increase vascular resistance throughout the cortex.