Influence of lysine-vasopressin dosage on the time course of changes in renal tissue and urinary composition in the conscious rat

1. The changes in urinary and renal tissue composition induced by continuous, intravenous infusion of lysine-vasopressin (2.5, 5, 15 and 60 mu-u./min. 100 g body wt.) for up to 4(1/2) hr in water-loaded, conscious rats were determined.2. Both the magnitude of, and the time required to attain, maximal and stable responses, in respect to both urinary and tissue composition, varied with the dose.3. The dose-dependent changes in medullary composition were compounded of graded decreases in water content and graded increases in solute (mainly Na and urea) content.4. The relative contribution of the changes in water, Na and urea contents varied with time and with dose. Significant increases in papillary urea content occurred with all doses. The range of change in urea content was wider than that for any other solute.5. At low doses, the changes in urinary flow and osmolality were ascribable, almost entirely, to large decreases in free-water clearance, with minor changes in medullary composition; at higher doses, the increases in urinary osmolality were accompanied by steep increases in medullary solute concentrations.6. A variable, dose-dependent, transient natriuresis occurred during the phase of increasing medullary Na concentration; the peak natriuresis preceded the times of maximal osmolal and Na concentrations in the papilla and urine.7. The differences in osmolal, urea and Na concentrations between papilla and urine also changed with time.8. Both the transitional and steady-state changes induced by lysine-vasopressin are discussed in terms of intrarenal mechanisms. It is concluded that the data are most reasonably interpreted on the basis that several hormone-sensitive loci exist in the kidneys, each with individual dose-response and kinetic characteristics.     

Time course of changes in renal tissue and urinary composition after cessation of constant infusion of lysine vasopressin in the conscious, hydrated rat

1. The changes in urinary and renal tissue composition in conscious rats were determined for up to 2 hr following the cessation of intravenous infusion of lysine vasopressin, LVP (at 60 muu./min. 100 g body wt. for 4(1/2) hr). A constant water load (4% body wt.) was maintained during and after lysine vasopressin infusion, by quantitative replacement of excreted water. In these circumstances, any changes in urinary and renal tissue composition are presumed to represent direct consequences of the rapid plasma and tissue clearance of lysine vasopressin.2. Urinary flow increased and osmolality decreased, rapidly, reaching stable values characteristic of sustained water diuresis after about 60 min.3. The steepness of the corticomedullary solute concentration gradients also decreased rapidly. Papillary Na and urea concentrations fell to values characteristic of sustained water diuresis in about 45 min.4. The changes in medullary composition were compounded of a moderate significant increase in water content, a moderate, significant decrease in Na content, and a profound decrease in urea content.5. In the eventual steady-state water diuresis, urinary outputs of Na and K were significantly lower, and of NH(4) significantly higher, than those observed in control experiments where LVP infusion was continued for the corresponding 2 hr.6. It is concluded that the diuresis following the cessation of LVP infusion is due not merely to reduced nephron permeability to water but also to a rapid reduction in the osmotic force responsible for water reabsorption from the collecting duct.     

Primate kidney function in hemorrhagic shock as influenced by dibutyryl cyclic AMP.

Standardized hemorrhagic shock was employed to study alterations in electrolyte and water handling in the owl monkey, either normally hydrated or moderately dehydrated. Increase in fractional clearance of osmolarity,sodium, and calcium occurred with retransfusion after the hypotensive phase. In the hydrated animals, free-water clearance became positive, and the urine-to-plasma osmolarity ratio [(U/P)osM] decreased below 1.0. In the dehydrated animals, free-water reabsorption (TCH2O) decreased but remained negative,while (U/P)osM remained above 1.0. Dibutyryl cyclic AMP (DBcAMP) was infused into the renal arterial supply in an attempt to correct a possible deficiency of cyclic AMP production. In the hydrated group, free-water clearance (CH2O) became more positive with infusion, and (U/P)osM decreased even further, with no effect on fractional sodium clearance. Effects were less or absent in the dehydrated group. Possible explanations for the observed effects of DBcAMP are considered. It was concluded that the loss of concentrating power seen in hemorrhagic shock occurs at a step beyond the production of cyclic AMP by adenylate cyclase.     

Hepatic osmoreceptors?

1. The effects of 0.45% saline infusions into the portal vein of conscious and anaesthetized dogs have been compared with similar infusions through a systemic vein.2. Measurements were made of plasma and urinary osmolality, sodium, potassium and chloride concentrations and urine flows; osmolal clearances, free water clearances, the percentage of the infused loads excreted at given times, and rates of sodium and potassium excretion in the urine, were calculated.3. In the conscious and anaesthetized series of experiments no significant differences were found between the portal and systemic routes of infusion.4. For both the portal and systemic routes of infusion there was a significantly smaller diuretic response to the saline infusion in anaesthetized as compared with conscious animals.5. These results do not support the concept of hepatic osmoreceptors occurring in the dog.     

Influence of prehydration on the changes in renal tissue composition induced by water diuresis in the rat

1. The composition of renal tissue was determined in rats before and immediately after intravenous infusion of dextrose (2.5 g/100 ml.) in amounts sufficient to administer a positive fluid load of 4% body weight over 2 hr. The rats were classified into three groups, according to the preinfusion urine osmolality: hydropaenia, normal and moderately diuretic (over 2400, 800-1500 and below 800 mu-osmoles/g H(2)O, respectively).2. In non-infused rats, the steepness of the corticomedullary osmolal gradient varied, due to differences in both water and solute (sodium and urea) contents, and was related to urinary osmolality. Whereas differences in medullary and papillary solute contents occurred between all three groups, papillary water content was significantly higher only in the moderately diuretic animals.3. Dextrose infusion caused the induction of water diuresis, the lowest urinary osmolalities being produced in the previously moderately diuretic animals.4. Dextrose infusion caused a considerable reduction in the steepness of the corticomedullary osmolal gradient in all rats, particularly in the previously hydropaenic animals, due to changes in both solute (sodium and urea) and water contents. Whereas reductions in medullary and papillary solute contents occurred in all three groups, there was no further increase in papillary water content from the already high values seen in the noninfused diuretic animals.5. Thus, dextrose infusion largely abolished any previous differences in tissue water content, whereas significant, though small, differences in osmolal (particularly urea) content persisted.6. These data are discussed in terms of changes and differences in endogenous antidiuretic hormone (A.D.H.) release.7. Changes in the magnitude and direction of the urinary-papillary urea concentration difference are discussed in terms of passive transport, with probable A.D.H.-induced changes in nephron urea permeability.     

Urine concentration during solute diuresis in potassium-depleted rabbits. Evidence for a defect in tubular sodium transport

1. The relationship between osmolal clearance (C(osm)) and the reabsorption of solute-free water by the kidney (T(H2O) (c)) was examined during 10% mannitol and 2.3% saline diuresis in normal and potassium-depleted rabbits.2. In normal rabbits at osmolal clearances close to 3.0 ml./min, T(H2O) (c) during mannitol diuresis was 0.87 +/- 0.06 ml./min and during saline diuresis 1.19 +/- 0.07 ml./min. The mean difference in T(H2O) (c) of 0.32 +/- 0.05 ml./min was highly significant (P < 0.001).3. In one group of potassium-depleted rabbits with a reduction in maximal urinary concentration, T(H2O) (c) during both mannitol and saline diureses was reduced significantly below normal and the increment in T(H2O) (c) normally seen during saline diuresis was abolished.4. In a second group of potassium-depleted rabbits maximal urinary concentration (1253 +/- 88 m-osmole/kg H(2)O) was not significantly different from that in normal rabbits (1272 +/- 116 m-osmole/kg H(2)O). In these animals, T(H2O) (c) at osmolal clearances close to 3.0 ml./min was not significantly different during mannitol diuresis (0.83 +/- 0.07 ml./min) from that in normal animals, whereas it was reduced significantly during saline diuresis (0.89 +/- 0.07 ml./min, P < 0.001) and the difference in T(H2O) (c) normally seen between mannitol and saline diuresis was abolished.5. The inability to increase T(H2O) (c) during saline diuresis above that achieved during mannitol appears to be the earliest manifestation of the concentrating defect associated with potassium depletion. It probably results from an impairment of sodium transport by the ascending limb of the loop of Henle. This is supported by the fact that potassium-depleted rabbits excreted a greater percentage of the filtered load of sodium than did normal controls.     

Effects of 0·9% saline infusion on urinary and renal tissue composition in the hydropaenic, normal and hydrated conscious rat

1. Changes in water and solute outputs of hydropaenic, normal and hydrated conscious rats were determined during intravenous infusion (0.2 ml./min) of isotonic (0.9%) saline for 4 hr; renal tissue composition was determined before, and after 1 or 2 hr, infusion.2. In normal and hydrated rats increased excretion of water and sodium was such that urinary output matched intravenous input from about 2 hr. In hydropaenic rats, the diuretic and natriuretic response was much reduced; a retention of infused saline, equivalent to 15% body weight, occurred over 4 hr.3. A considerable increase in urea output and clearance, and a smaller increase in potassium and ammonium outputs, occurred in all groups.4. The corticomedullary osmolal gradients characteristic of non-diuretic rats were largely dissipated during saline infusion: by 1 hr in normal and hydrated rats, and by 2 hr in the hydropaenic group.5. These changes were ascribable mainly to an increase in tissue water content in all segments, particularly in the hydropaenic group; and to a profound decrease in urea content in all groups.6. Changes in tissue sodium content were smaller, and differed between segments and between the differently hydrated groups. A decrease in papillary content occurred in hydropaenic and normal groups and an increase in cortical and outer medullary content occurred in all groups.7. After 2 hr saline infusion, incomplete papillary-urinary osmotic equilibration was evident in all groups.8. These changes in medullary osmolality and in papillary-urinary osmotic equilibration preceded the maximal diuresis, and must contribute to the diuresis induced by saline infusion, as in water and osmotic diureses.     

Comparison of renal responses to 5% saline infusions into vena portae and vena cava in conscious dogs

Indwelling catheters were placed in conscious dogs into the vena portae via a jejunal mesenteric vein several weeks prior to actual experiments. To compare a possible different response to different pathways of administration, 5% saline solution was infused either into vena portae or into vena cava at a rate of 0.05 ml/min/kg BW for 40 min.

1. Infusion of 5% sodium chloride into the vena portae, as well as into the vena cava caused a significant increase in urine flow, serum osmolality, sodium excretion rate and heat rate. The increase in urine flow was always due to an increase in osmolal clearance whereas free water clearance decreased consistantly. In some experiments plasma renin activity (PRA) was measured by radioimmunoassay. For both routes of administration the hypertonic saline infusion caused a decrease in PRA. At no time did any of these parameters display significant differences depending on route of application.
2. This means that the calculated differences between infused and excreted amounts of water and of sodium did not depend on the route of infusions.
3. A close relationship was found between initial urine osmolality and the length of the periods during which peak values of urine flow were observed.

These results do neither provide evidence for a hepatic osmoreceptor mechanism in dogs nor for the hypothesis that in conscious dogs the liver might control sodium excretion.     

Water handling by the sabra hypertension prone (SBH) and resistant (SBN) rats

The renal handling of water by SBH and SBN rats was evaluated under basal conditions and following various intervention procedures. During 17 weeks of unrestricted water intake, SBH rats drank less water and excreted less urine with a higher osmolality than SBN. The differences in urine volume and osmolality persisted during 2 weeks of paired water intake. Acute water loading elicited comparable dilution of the urine in the two strains. Water deprivation for 48 h resulted in a marked rise in urine osmolality, which tended to be higher in SBN. Administration of exogenous vasopressin in water loaded animals caused a similar rise in urine osmolality. Papillary solute and urea content was higher in SBH than in SBN, but comparable in water loaded animals. The results show that although SBH differ from SBN rats in the handling of water under basal conditions, their renal diluting and concentrating capacity is comparable at extreme conditions. GFR and RBF were equal in both strains. The data suggest that SBH rats have increased renal water reabsorption as compared to SBN, which may be mediated by ADH, PG or other mechanisms. This characteristic may be related to their propensity to develop hypertension.     

Renal function in sheep during infusion of alkali metal ions into the renal artery.

1. The effect on renal function of 1 M solutions of LiCl, NaCl, KCl, RbCl and CsCl and 3 M-NaCl infused close-arterially to the kidney for 10 min at 0-7ml./min has been studied in nine experiments on four unilaterally nephrectomized sheep. The levels of flow, electrolyte concentration and electrolyte excretion in the urine were measured before, during and for 50 min after the infusions. 2. The infusion of 1-M-NaCl produced little change in urine flow and composition whereas 3 M-NaCl resulted in relatively small increases in urine flow and sodium excretion. 3. The infusion of lithium, potassium, rubidium and caesium resulted in marked increases in urine flow, urinary sodium concentration and excretion, urinary potassium excretion and osmolal clearance while the urinary potassium concentration decreased. 4. Changes in urine flow and urinary pH during the infusions of all the alkali ions except sodium were consistent with increased urinary bicarbonate excretion. 5. The osmolal clearance was increased by the infusion of lithium, potassium, rubidium and caesium, but equivalent increases in the rate of solutefree water reabsorption did not occur. 6. The infusion of caesium resulted in a depression of the glomerular filtration rate (G.F.R.) which was not observed when the other alkali ions were infused. 7. The effects of lithium, potassium and rubidium on urine flow and composition were rapid in onset and the residual effects on these ions, on cessation of infusion, were relatively short. The effects on caesium were slow in onset and prolonged in duration. 8. It was concluded that lithium, potassium, rubidium, and caesium altered urine flow and electrolyte excretion by acting upon common mechanisms which were predominantly intra-renal and located in the proximal segment of the nephron.     

Suppressive action of prolactin on renal response to volume expansion.

The effects of prolactin on rat renal sodium and water handling during volume expansion were studied using clearance techniques. Both control and experimental adult male Wistar rats were prehydrated with an oral water load of volume equal to 2.5% body weight (BW). At least 3 h later, a continuous intravenous infusion of ovine prolactin (NIH-P-S8), 7.1 mug/h per 100 g, was started in the experimental group. After a 1-h steady-state period, the rats were given an intravenous expansion infusion of either hypotonic saline (2.5% BW), isotonic saline (2.5% and 7.5% BW), or blood (2.5% BW). In all control hypotonic and isotonic saline-expanded animals, within 1 h the rats excreted a volume of urine equal to over 50% of the volume of saline infused. The diuretic and natriuretic responses to saline expansion of prolactin-treated rats were significantly smaller than controls. In contrast to the effects of prolactin on the renal response to saline infusions, it did not alter the natriuretic or diuretic response to blood infusion. Prolactin may be counteracting the effects of physical factors on the regulation of sodium reabsorption in the proximal tubule.     

AQP3 缺失小鼠尿素和尿浓缩能力的研究

目的： 肾脏表达水通道蛋白3（AQP3）在尿浓缩机制中起着极其重要的作用。AQP3缺失小鼠表现为尿浓缩功能严重障碍。为阐明这种基因缺失的生理特性和发生机制,我们利用AQP3基因敲除小鼠和野生型小鼠复制急性尿素负荷动物模型,对其作用机制及影响进行研究。方法: 对小鼠实施急性尿素负荷,从实验前2 h到尿素负荷后第8 h,每隔2 h收集1次尿样分别检测尿量、尿渗透压及尿素浓度。分离肾脏组织RNA进行实时荧光定量RT-PCR反应。应用Western blotting分析肾组织中尿素转运蛋白（UTs）的变化。结果: 给予尿素后4 h左右,2种不同基因型小鼠均有负荷尿素的排泄。尿素负荷后AQP3缺失小鼠尿的渗透压和尿素含量逐渐增高,第 8 h,几乎与野生型小鼠值相等,但尿中非尿素溶质浓度却没有改变。在最后4 h内尿量下降到基础值的1/4。AQP3基因缺失和野生型小鼠尿素负荷显著地上调了UT-A3的表达。结论: AQP3基因缺失并没有直接干扰肾脏对尿素的浓缩功能,但却减弱了对尿中其它溶质浓缩的能力。这种对溶质选择性的反应是由于AQP3对水和尿素转运能力的不同所致。结果表明AQP3对尿中非尿素溶质的浓缩具有特殊作用。     

Effect of angiotensin II on renal water excretion.

In the present study the effect of angiotensin II (AII) on renal water excretion was evaluated. In dogs undergoing a water diuresis, neither the intravenous (IV) (40ng/kg per min) nor intracarotid (5-10 ng/kg per min) infusion of AII significantly altered urinary osmolality (Uosm) or free-water clearance (CH2O). Intravenous infusion of a competitive inhibitor of AII (1-sarcosine,8-glycine AII) into hydropenic dogs also failed to alter Uosm and CH2O significantly. To examine whether AII might suppress, rather than stimulate, vasopressin release, AII was also infused into hydropenic animals. No effect on Uosm and CH2O was observed during the intracarotid infusion. A significant fall in Uosm and rise in CH2O occurred during the intravenous AII infusion, but reversal after cessation of the infusion was incomplete and statistically not significant. Some suppression of antidiuretic hormone (ADH) release during the intravenous infusion of AII, however, was suggested since no similar alteration in renal water excretion was observed during an intravenous AII infusion in hypophysectomized animals receiving a constant infusion of ADH. Taken together, the present results provide no evidence for a direct effect of AII to alter ADH release or to interfere with the peripheral action of ADH. Suppression of ADH release may sometimes occur with pressor doses of intravenous angiotensin, but this effect is clearly less consistent than previously observed with intravenous norepinephrine.     

Amino acid transport in isolated hepatocytes after partial hepatectomy in the rat.

The effect of partial (70%) hepatectomy on amino acid transport was investigated by measuring the uptake of the nonmetabolizable amino acid analogue alpha-amino-[1(-14C]isobutyric acid in hepatocytes freshly isolated from the liver remnant. In hepatocytes from partially hepatectomized rats, both the influx and the efflux of alpha-aminoisobutyric acid were increased. Quantitative analysis of the relationship between the initial rate of uptake and the substrate concentration indicated that a high-affinity component was responsible for the increased rate of amino acid entry in hepatocytes from partially hepatectomized rats. This component could be detected 90 min after operation, but its Vmax increased with time. The high-affinity component was strictly dependent on sodium and had the properties of a pure A system; its mode of energization partly involved cationic transmembrane gradients. The L system of amino acid transport was not affected after partial hepatectomy. The rapid emergence of a high-affinity amino acid transport system in the liver remnant following partial hepatectomy may play an important role in the regulation of liver regeneration.     

Importance of tubulo-interstitial changes in glomerular excretory and urine concentrating function of the kidney

Results are presented for morphologic investigations on the correlation between structural and functional alterations in various inflammatory and non-inflammatory glomerular and extraglomerular renal diseases. The role of the glomeruli in the excretion of substances excreted exclusively by the urinary tract is dependent, to a degree not previously appreciated, on the condition of the postglomerular vasculature as well as on the functional status of the tubular epithelium. All processes which result in damage to the post-glomerular vasculature negatively influence glomerular excretory function by limiting the flow of blood out of the glomeruli and reducing glomerular perfusion. It is further assumed that all processes which negatively influence tubular reabsorption will also be detrimental to glomerular function as a result of increased pressure in the proximal renal tubule as well as via the Thurau mechanism. Finally it is suggested that the kidney's concentrating ability is partially dependent on tubular interstitial factors: with increasing width of the renal cortical interstitium and increasing atrophy of the renal tubule (as measured by the proximal tubules) the kidney's concentrating ability steadily diminishes.     

A central osmosensitive receptor for renal sodium excretion.

1. The effect on renal Na and water excretion of increasing the NaCl concentration of blood supplying the brain was investigated in conscious water-loaded sheep. Intracarotid infusion ot 4 M-NACl at 0-8 ml./min for 60 min was compared with equivalent intrajugular infusion. 2. A more rapid increase in renal Na excretion and urine osmolality occurred with the intracarotid infusions than with intrajugular infusions. 3. Intracarotid infusions of 2 M sucrose or fructose at 1-6 ml./min for greater increase in renal Na excretion, urine osmolality and a decrease in urine flow rate. 4. The results suggest that there are receptors in the brain sensitive to changes in extracellular tonicity which influence renal Na excretion. It is possible that changes in ADH secretion alone mediate the early natriuresis seen with intracarotid hypertonic infusions although an alternative concurrent mechanism cannot be ruled out.     

Urea reabsorption in the medullary collecting duct of protein-depleted young rats before and after urea infusion

The aims of the present study were to examine urea handling along the length of the medullary collecting duct (MCD) in protein-depleted young rats and to determine the effect of urea infusion on MCD function and urine concentrating ability. In 10 young rats on a low protein diet, urea reabsorption equivalent to 18.3% of the filtered load was observed along the MCD (4.5 mm) using the microcatheterization technique. Collecting duct urea reabsorption occurred almost entirely (16.6%) in the distal portion of the MCD (mid-zone to papillary tip, 2.8 mm). These results are in contrast to the lack of net urea reabsorption along the MCD in protein-replete adult rats [21]. After urea infusion which raised plasma urea level from 3.5 to 10.5 mmol/l in protein-depleted rats, urine non-urea solute concentration increased in the non-exposed right kidney from 827 to 1,199 mosm kg^–1 (P<0.001) but the increase was not significant in the experimental left kidney (590 to 619 mosm kg^–1). Thus exposure of the papilla interfered with urea-induced enhancement of urine concentrating ability. After urea infusion, fractional urea reabsorption in the distal portion of the MCD was similar to that before infusion (21.1%) of filtered load) but the absolute load of urea delivered to the MCD and reabsorbed along the duct was markedly increased (2.7-fold). In 6 rats with an increase in urine non-urea solute concentration in the experimental kidney after urea infusion, fluid reabsorption along the duct was significantly increased. The results indicate that in protein-depleted young rats (1) there is significant urea reabsorption in the distal portion of the medullary collecting duct, (2) urea infusion contributes to enhanced urine concentrating ability, in part, by increasing absolute urea reabsorption and also water reabsorption in the collecting duct.     

Difference between hypertonic NaCl and NaHCO3 as osmotic diuretics in dog kidneys

To compare the osmotic inhibitory effects of NaCl and NaHCO3 on proximal tubular fluid reabsorption, plasma osmolality was raised by 40 mosmol kg-1 H2O by infusing hypertonic NaCl and NaHCO3 in volume-expanded dogs receiving ethacrynic acid. In five dogs studied at constant plasma pH 7.5, both NaCl and NaHCO3 reduced water reabsorption by 29 +/- 2%. However, NaCl infusion reduced bicarbonate reabsorption by 31 +/- 2%, whereas bicarbonate reabsorption remained unchanged during NaHCO3 infusion. In six dogs, bicarbonate reabsorption was kept constant during NaCl and NaHCO3 infusion by adjustments of plasma pH. At similar glomerular filtration rates (42.4 +/- 2.9 ml min-1), water reabsorption was 28.7 +/- 1.7 ml min-1 in the control period, 29.4 +/- 2.5 ml min-1 during hypertonic NaCl infusion and 20.6 +/- 1.2 ml min-1 during hypertonic NaHCO3 infusion. Therefore, NaCl did not reduce proximal tubular water reabsorption by a direct osmotic effect. By calculating the regression coefficient for the relationship between measured chloride reabsorption and maximal convective chloride flux, the effective reflection coefficient for NaCl averaged 0.11 +/- 0.01. The combination of a low reflection coefficient and high permeability may explain why hypertonic NaCl is not an osmotic diuretic.     

Quantitation of renal uric acid synthesis in the chicken

The contribution of uric acid synthesized in the kidney (nephrogenic uric acid) to the total uric acid excreted in the urine was studied in the chicken by use of the isotope-dilution technique. In the non-fasted chicken the urine-to-plasma specific activity ratio (SAR) of [14C]uric acid was 0.83, suggesting that a minimum of 17% of the uric acid excreted in the urine is synthesized in the kidney. During allopurinol infusion into the renal portal circulation of one kidney the SAR increased to 0.99, indicating that the renal synthesis of uric acid was almost completely inhibited and that the SAR is a valid indicator of the contribution of nephrogenic uric acid excreted into the urine without first entering the circulation. Chickens fasted for 18 h showed a lower rate of renal synthesis of uric acid. Hypoxanthine infusion into the systemic circulation increased the rate of renal synthesis of uric acid in both fasted and nonfasted chickens, suggesting that circulating precursor levels may in part regulate the renal synthesis of uric acid.     

Increased urinary kallikrein excretion during prostaglandin E1 infusion in anaesthetized dogs and its relation to natriuresis and diuresis.

. The effect of intra-arterial prostaglandin E1 (PGE1) infusion on urinary kallikrein, sodium, potassium and water excretion was studied in normal anaesthetized dogs. 2. Infusion of PGE1 caused a dose-related increase in urinary excretion of kallikrein, sodium, potassium and water as well as an increase in renal blood flow (R.B.F.) and a fall in urinary osmolality and renal vascular resistance. 3. The changes occurred in the absence of appreciable changes in inulin clearance (Cin), arterial blood pressure, haematocrit, and plasma sodium and potassium concentrations. 4. The increased urinary kallikrein excretion correlated positively with the natriuresis, diuresis and kaliuresis and the increase in renal blood flow, but negatively with the urinary osmolality and renal vascular resistance. 5. It is concluded that renal kallikrein is involved in the renal response to arterial infusion of PGE1.