Correlation between luminal hydrostatic pressure and proximal tubular fluid reabsorption in the rat kidney

Summary Split-drop experiments were performed to evaluate the effect of changes in luminal hydrostatic pressure on net fluid reabsorption in proximal convoluted tubules of the rat kidney. While hydrostatic pressure in control droplets averaged 28.9±1.03 mm Hg, it increased to a mean of 65.2±3.3 mm Hg during pressure elevation and fell to 10.8±1.04 mm Hg during pressure reduction. In paired measurements in identical tubules net fluid absorption changed from a control value of 2.96±0.14 nl/min·mm to 3.88±0.14 nl/min·mm when luminal pressure was elevated. During pressure reduction net fluid absorption fell from a control of 2.98±0.09 nl/min·mm to 2.26±0.13 nl/min·mm (P<0.001). This dependency of fluid absorption upon hydrostatic pressure was not greatly affected by the finding that microphotography overestimated the true intradroplet volume by 31% during control and by 30.2% and 50% during elevated and reduced pressure respectively. From the relation between the changes of net absorption and luminal hydrostatic pressure an apparent hydraulic conductance of 0.04 nl/min·mm Hg was estimated.     

Peritubular capillary control of proximal tubule reabsorption in the rat.

Changes in peritubular capillary hydrostatic and oncotic pressures, which probably affect net interstitial pressure and, thus, the force on fluid movement across the tubule basement membrane, can modulate absolute proximal reabsorption rate (APR). To examine the relationship between APR and net interstitial pressure, we measured peritubular capillary hydrostatic and oncotic pressure, single nephron filtration rate, APR, absolute distal reabsorption (ADR), and tubular hydrostatic pressure in hydropenic, saline-loaded, and plasma-loaded rats. Net interstitial pressure in saline loading was estimated from subcapsular hydrostatic pressure and lymph protein concentration measurements. The surface area-hydraulic conductivity product of the peritubular capillary network was estimated from these measurements with a model of capillary fluid exchange in which fluid uptake was defined to be APR plus ADR. The estimated value was assumed to remain constant in all three states, and was then used to estimate net interstitial pressure in hydropenic and plasma-loaded rats. APR and net interstitial pressure correlated strongly, a finding consistent with the hypothesized role for net interstitial pressure in regulating proximal reabsorption.     

Changes in interstitial pressure during and after blood volume expansion in rats

Summary Interstitial fluid pressure was measured via a chronically implanted capsule before, during and after acute isotonic, iso-oncotic blood volume expansion in normal or in 48-h dehydrated rats. At the same time, the patterns of body fluid distribution, of selected renal responses and of mean arterial and mean central venous pressure responses were studied. Dry tissue weight (DTW) was subsequently determined by freeze drying of the shaved carcass.Dehydration decreased plasma volume and interstitial fluid volume significantly below normal values. The initial intracapsular pressure in dehydrated animals (–3.7±0.6 mm Hg) was not significantly different from that in normal rats (–2.5±0.5), but dehydrated rats showed initially a very significantly lower effective interstitial compliance (0.0005 ml/mm Hg per gram DTW) than did the normal group (0.0704).In the course of the renal response to the volume load, effective interstitial complicance increased to 0.0350 in dehydrated rats but showed no change in normal rats. Neither group completely corrected its elevated blood volume; both returned their central venous pressures to pre-infusion levels; both decreased their interstitial fluid volumes below preinfusion levels and both decreased their intracapsular fluid pressures 1 mm Hg below the level prevailing in non-infused animals at that time.It is concluded that a reduction in interstitial, hydrostatic pressure can be a functionally important influence in the apparent control of central venous pressure following acute blood volume expansion.This study was supported by the Canadian Heart Foundation.     

Modulation of proximal tubular hydraulic conductivity by peritubular capillary oncotic pressure

Fluid absorption from the proximal tubular lumen is probably a multifactorial process. Earlier studies from our laboratory have indicated that a transepithelial hydrostatic and oncotic pressure difference may be the driving force for as much as 30% of the reabsorbed fluid. During saline volume expansion proximal tubular reabsorption declines and the present experiments were undertaken to investigate whether this reduction could be caused by changes in the passively driven flux component. The hydraulic conductivity was therefore determined from the reabsorptive rate in split oil droplets with normal and high hydrostatic pressure gradients across the wall, at the same time as the peritubular capillary net-work was perfused with solutions containing a colloid of high or low concentration. In the reabsorption experiments the split oil droplet radius was measured and in a separate series of experiments the relationship between droplet radius and pressure was determined; this was found to be 7.3 mmHg pressure increase per 1 μm increase in radius. The increase in the rate of reabsorption from the droplets due to increased intraluminal hydrostatic pressure was 1.02±0.13 nl/min/mm tubular length when a solution with a high colloid concentration was perfused through the capillary net-work, compared with 0.41=0.11 nl/min/mm tubular length when a low colloid containing solution was used for perfusion. The hydraulic conductance in the proximal tubular wall at high colloid perfusion was calculated to be 0.54 nl/min mm mmHg while at a low capillary colloid oncotic pressure it was significantly lower 0.025 nl/min mm mmHg. This drop in hydraulic conductance might be one factor responsible for the decline in fluid absorption in animals exposed to saline volume expansion.     

Kinetics of the Glomerular Ultrafiltration in the Rat Kidney. A Theoretical Study

The glomerular filtration process was evaluated theoretically from micropuncture data obtained from Sprague-Dawley rats. The hydrostatic pressures in the glomerular capillaries and Bowman's space minus the oncotic pressure in systemic plasma gave the net driving force at the proximal end of the glomerular capillary. From the single nephron filtration fraction the mean net driving force over the glomerular membrane was calculated to be 20 mm Hg during normotension, decreasing to 12 mm Hg during a perfusion pressure of 80 mm Hg. The hydraulic permeability for one glomerulus was 0.7-0.8 nl/min. 100g b. wt. mmHg. The pressures at the distal end of the glomerular capillaries were 13 and 6 mm Hg under the above two conditions, indicating non-equilibrium of the filtration process at the end of the glomerular capillary. It was shown that the glomerular filtration rate is mainly influenced by the driving pressures. During hypotension an increased plasma flow dependency was evident. Brenner et al. found a filtration equilibrium and a plasma flow dependent glomerular filtration rate in a mutant Wistar rat strain. The discrepancy between their results and ours is due to the low glomerular plasma flow and hydrostatic pressures in the Wistar rats. It is concluded from our results that both pre- and postglomerular resistances may influence the glomerular filtration rate and glomerular plasma flow independently.     

Determinants of peritubular capillary fluid uptake in hydropenia and saline and plasma expansion.

Hydrostatic (HPc) and oncotic (phic) pressures within the peritubular capillary, tubular pressure (Pt), nephron filtration rate, and plasma flow, and proximal fractional and absolute reabsorption (APR) were measured in anesthetized rats during hydropenia and plasma and saline expansion. Net interstitial pressure (phii-HPi) was estimated from subcapsular hydrostatic and oncotic pressures during saline expansion and these data were applied to a mathematical model of peritubular capillary fluid uptake to determine the profile of effective reabsorption pressure (ERP) with distance (x*) alongthe capillary and calculate the peritubular capillary permeability coefficient (LpAr). ERPX* = (PHIC MINUS HPC)X* MINUS (PHII MINUS HPi) and APR = ERPX*LpAr.During saline expansion phii minus HPi was -12.1 plus or minus 0.8 mmHg and ERP,3.8 mm. The LpAr was 0.07 nl/s per g KW per mmHg, and this value was applied to hypropenia and plasma expansion to determine ERP and phii minus HPi. The phiiminus HPi was +6.0 and +5.0 mmHg, respectively, and ERP was 4.1 and 3.5 mmHg.Efective reabsorptive pressure remained positive along x* in all states, and phii minus HPi correlated best changes in phic and poorly with changes in efferent plasma flow. The APR did not correlate with either calculated phii minus HPi or the transepithelial driving pressure, Pt + phii minus HPi.     

Kinetics of the glomerular ultrafiltration in the rat kidney. A theoretical study.

The glomerular filtration process was evaluated theoretically from micropuncture data obtained from Sprague-Dawley rats. The hydrostatic pressures in the glomerular capillaries and Bowman's space minus the oncotic pressure in systemic plasma gave the net driving force at the proximal end of the glomerular capillary. From the single nephron filtration fraction the mean net driving force over the glomerular membrane was calculated to be 20 mm Hg during normotension, decreasing to 12 mm Hg during a perfusion pressure of 80 mm Hg. The hydraulic permeability for one glomerulus was 0.7-0.8 nl/min-100 g b.wt. mmHg. The pressures at the distal end of the glomerular capillaries were 13 and 6 mm Hg under the above two conditions, indicating non-equilibrium of the filtration process at the end of the glomerular capillary. It was shown that the glomerular filtration rate is mainly influenced by the driving pressures. During hypotension an increased plasma flow dependency was evident. Brenner et al. found a filtration equilibrium and a plasma flow dependent glomerular filtration rate in a mutant Wistar rat strain. The discrepancy between their results and ours is due to the low glomerular plasma flow and hydrostatic pressures in the Wistar rats. It is concluded from our results that both pre- and postglomerular resistances may influence the glomerular filtration rate and glomerular plasma flow independently.     

Hydrostatic and oncotic pressures in the interstitium of dehydrated and volume expanded rats

The pressures in the renal interstitial space seem to have important influence on the setting of the sensitivity of the tubuloglomerular feedback that controls the glomerular filtration rate (GFR), and on the rate of proximal tubular fluid reabsorption. Measurements were made of interstitial pressure conditions, GFR, renal plasma flow (RPF), urinary excretion of sodium and potassium, and plasma renin activities in dehydrated animals and normopenic controls, before and after saline volume expansion (5% of body weight and hour). Colloid osmotic pressure, estimated from the protein concentration in renal hilar lymph, was 7.5 mmHg in the dehydrated animals (controls 2.8 mmHg) and decreased to 3.1 (controls 1.7 mmHg) after volume expansion. The lymph flow rate was increased in both groups of animals after volume expansion. Interstitial hydrostatic pressure, measured in the subcapsular space, was 2–3 mmHg in dehydrated and control animals and increased to 3–4 mmHg after volume expansion. In dehydrated rats GFR and RPF was reduced to 60% of the control values, but after volume expansion they regained control values. After volume expansion, urinary excretion of fluid and electrolytes increased more in controls than in dehydrated rats. Plasma renin activity was dereased in both groups of rats after volume expansion. Thus, in dehydrated animals there was a high colloid osmotic pressure and a low hydrostatic pressure in the renal interstitium, while after volume expansion the oncotic pressure fell and the hydrostatic pressure rose. The effect of volume expansion was found to be dependent on the preceding volume balance situation in the animal.     

Tubuloglomerular feedback in hypertensive rats of the Milan strain

In rats of the Milan hypertensive strain (MHS) the disease can be transplanted with the kidney to rats of the Milan normotensive strain (MNS). It has been found that GFR, salt and volume regulation differ between MHS and MNS rats. Tubuloglomerular feedback control mechanism (TGF) is important for body volume regulation and we therefore wanted to study the TGF control in MHS and MNS rats. Whole kidney and micropuncture experiments were done before and during saline volume expansion (5% of body weight). In an initial series of experiments measurements were made of total kidney GFR, urine excretion rate of sodium and potassium and subcapsular interstitial hydrostatic pressure (psc); interstitial oncotic pressure (pi int) was estimated from hilar lymph protein concentration. In a second series, proximal tubular stop-flow pressure (psf) was determined upstream from a wax block while the distal nephron was being perfused with Ringer solution at a flow rate varying from 0 to 40 nl X min-1. In this way the maximal drop in stop-flow pressure (delta psf) and also the turning point (TP), the tubular flow rate at which 50% of this response was achieved, could be determined after saline volume expansion and after 2 h of complete ureteral occlusion. The results showed that GFR was similar in MHS and MNS rats in the control situation, but that during volume expansion it was significantly lower in the MHS group. Interstitial psc and pi int and net interstitial pressure (psc - pi int) were similar in MHS and MNS rats both under control conditions and during volume expansion.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hydraulic permeability of the peritubular and glomerular capillary membranes in the rat kidney

The hydraulic conductivity of the peritubular capillary membrane was calculated from I) single nephron fluid reabsorption and 2) net driving force, i. e. from hydrostatic and colloid osmotic pressures in renal interstitium and peritubular capillary blood, as determined by a micropuncture technique and with use of a computer-based model. Under control conditions the net driving force was estimated to be 15.4 mmHg and the hydraulic conductivity 1.04 nl/(mmHg) per 100 g rat. During extracellular volume expansion with 0.15 M saline, 4% and 10% of body weight, the net driving force decreased to 12.5 mmHg and 6.4 mmHg, respectively, whereas the conductivity increased to 1.85 and 3.14 nl/(min-mmHg) per 100 g rat. The reduction in net driving force was compensated by an increased hydraulic conductivity. In the glomeruli the net driving force for filtration increased from 14.2 mmHg under control conditions to 21.2 mmHg and 25.3 mmHg during saline expansion 4% and 10%, whereas the corresponding hydraulic conductivity decreased from 1.13 nl/(min-mmHg) per 100 g rat to 1.03 and 0.80 nl/(min-mmHg) per 100 g rat during the two expansions. During saline expansion the water permeability of the glomerular capillaries is decreased while that of the peritubular capillaries is increased. These changes in the water permeability will lead to retarded excretion of the excess fluid.     

Model of interstitial pressure as a result of cyclical changes in the capillary wall fluid transport.

Reported interstitial pressures range from -8 to +6 mm Hg in different tissues and from <-20 mm Hg in burned tissue or more than +30 mm Hg in tumors. We have tried to link interstitial pressure to the here proposed cyclical changes in the fluid transport across the capillary wall.In the presented model interstitial pressure is considered as an average of pressures in numerous pericapillary spaces. A single pericapillary pressure is a dynamic difference between the net outward (hydraulic pressure+interstitial colloid osmotic pressure) and inward (plasma colloid oncotic pressure) forces. Hence, dominating net outward forces would result in a positive pericapillary interstitial pressure, while stronger inward forces would produce negative pressures in the pericapillary space. All interruptions of blood flow leave some blood in capillaries with a normal oncotic pressure and no hydrostatic pressure that might act as a strong absorber of interstitial fluid until the blood flow is reestablished.Model assumptions for the systemic circulation capillaries include (a) precapillary sphincters can almost entirely stop the capillary flow, (b) only a minority of sphincters are normally open in the tissue, and (c) hydrostatic pressures in unperfused capillaries are similar to the pressures at their venous ends.The key proposal is that capillaries with closed precapillary sphincters along their entire length have low hydrostatic pressure of 10 to 15 mm Hg. This pressure cannot force filtration, so these capillaries reabsorb interstitial fluid from the pericapillary space along their entire length. In the open capillaries, hydrostatic pressure filtrates fluid to the pericapillary space along most of their length. Fluid enters, moves some 20 or 30 micrometers away and back to be reabsorbed at the same point. Closed periods are periods of intense fluid reabsorption, while the short open periods refill the space with fresh fluid. It can be calculated that subcutaneous tissue interstitial pressure values might develop if the closed periods are 1.14 to 2.66 times longer than the open periods. Positive interstitial pressures observed in some organs might develop if open periods are longer than the closed periods.High interstitial colloid pressure in lungs makes both perfused and unperfused capillaries absorptive, resulting in more negative values of lung interstitial pressure. The same model is used to explain interstitial pressure values in tumors, burned tissue and intestinal villi.     

Estimation of plasma volume from hematocrit and plasma oncotic pressure during volume expansion in dogs

Changes in hematocrit and plasma oncotic pressure were measured continuously during and after isotonic volume expansion in splenectomized dogs in order to test the potential of these types of measurements to predict changes in plasma volume. A volume of Ringer's solution amounting to 15% of the initial blood volume was infused over 10 min. At the end of the infusion, 54% of infused fluid remained within the intravascular space and 9% of the infused volume was retained within the intravascular space at 50 min after the end of the infusion. Hematocrit and plasma oncotic pressure decreased by 2.4% and 2.4 mmHg, respectively, at the end of infusion and then variables returned to their control levels gradually. Changes in plasma volume were estimated indirectly from hematocrit and plasma oncotic pressure based on the dilution of the erythrocytes and the protein. Highly significant correlations were observed between the measured plasma volume (Y) and the plasma volume (X) calculated from hematocrit (Y = 0.95X + 0.22, r = 0.96) and the plasma oncotic pressure (Y = 0.86X + 0.46, r = 0.91). We therefore conclude that either hematocrit and plasma oncotic pressure measured continuously are reliable parameters for predicting the time course of the plasma volume change during an isotonic volume expansion of up to 15% of the initial blood volume.     

Transcapillary fluid movement in human calf after drinking hypertonic saline

1. Transcapillary absorption of interstitial fluid was demonstrated with a pressure plethysmograph applied to the human calf after the ingestion of 200 ml. hypertonic (5.1%) saline. Capillary absorption began within 15 min after ingestion and lasted for about 2 hr. The maximum rate of absorption (0.019 ml./min. 100 ml. tissue) was attained 30-75 min after ingestion.2. The total amount of fluid absorbed into capillary blood vessels in the calf was 1.11 ml./100 ml. tissue. The amount of fluid thus absorbed in the whole body was estimated to be 677 ml.3. The capillary filtration coefficient (CFC) of the calf was also measured by the pressure plethysmograph. This was 0.0038 ml./min. mm Hg. 100 ml. tissue.4. The peak value of capillary absorption pressure was 5.2 mm Hg.5. The total osmotic pressure of the plasma rose by 12.6 m-osmole/kg H(2)O after ingestion. This rise was accompanied by transcapillary fluid absorption.6. The plasma protein concentration and packed cell volume were almost unchanged by ingestion, indicating that the plasma volume was unaltered.7. It was estimated that the net shift of fluid between intracellular and interstitial compartments during the period of transcapillary fluid absorption was very small.8. It is concluded that the volume of fluid moving from plasma into intestinal lumen is the same as that flowing from interstitial fluid into plasma, and that the transcapillary absorption is caused by a difference in osmotic pressure between the plasma and the interstitial fluid.     

Kinetics of the Glomerular Ultrafiltration in the Rat Kidney. An Experimental Study

The quantitative relation between the driving forces over the glomerular membrane and the glomerular plasma flow, on the one hand, and the single glomerular filtration rate (SNGFR), on the other, is still uncertain. Micropuncture measurements on Sprague-Dawley rats made it possible to calculate the net driving force over the glomerular membrane. The single glomerular plasma flow was determined from SNGFR and the single nephron filtration fraction (SNFF). The effective plasma flow was measured with PAH for total kidney and for superficial nephrons. The mean glomerular capillary pressure was found to be 62.6 mm Hg. The results indicate a net driving force of about 13 mm Hg at the distal end of the glomerular capillary. SNGFR was found to be 14.1 nl/min.100 g. SNFF amounted to about 0.27. The filtration fractions determined with the PAH method were in the same range. The results indicate a filtration disequilibrium, in contrast to those of Brenner et al. from measurements on a mutant Wistar rat strain. The filtration fractions seemed to be the same in all glomerular populations. It is clear that the SNGFR is pressure dependent. Our earlier findings of a nonautoregulation of the blood flow through the outer glomeruli were also confirmed.     

Renal interstitial pressure measured in the subcapsular space using an in vivo oncometer

Continuous measurements of renal interstital pressure are of importance for several reasons. The present paper describes an in vivo oncometer developed for this purpose. A piece of dialysis tubing was filled with a 0.15 M NaCl solution containing 5 g albumin 100 ml-1. For detecting the hydrostatic pressure inside the tubing, a thin catheter and a silver wire were inserted into it and both ends of the tubing were sealed with glue. The catheter and the silver wire were connected to a servo-nulling pressure device. The oncometer was then placed under the renal capsule. The pressure inside the dialysis tubing was pi onc+Psc-pi sc, and since pi onc was known, the net interstitial pressure (Pnet, i.e. Psc-pi sc) could be measured continuously in the subcapsular space. Measurements were made during (I) intravenous bolus injection of 2 ml of 0.9% NaCl, (2) saline expansion of 5% of body weight, and (3) elevation of renal venous pressure to 20 mmHg by clamping the renal vein. In the control situation, Pnet averaged-3.3 mmHg, a value in good accordance with findings in earlier studies in which the hydrostatic and oncotic pressure components have been measured separately. Following bolus injection of fluid, Pnet increased transiently by 2.6 mmHg, whereas volume expansion produced a permanent increase in Pnet of almost the same magnitude. During elevated renal venous pressure Pnet was unaffected, except for a minor increase on clamping and a minor decrease on release of the clamp. The results show that reproducible and accurate measurements of Pnet in the renal subcapsular space can be made with an in vivo oncometer.     

Hydrostatic pressure in the subcapsular interstitial space of rat and dog kidneys

Summary Experiments were performed in rats and dogs in order to reevaluate the concept of a high renal interstitial pressure. Assuming that the renal subcapsular pressure represents the pressure 2 of the superficial interstitium, catheters were implanted in the subcapsular space and the pressure was continuously recorded with a transducer of a very low volume displacement. In 17 rats a mean subcapsular pressure of 3.8 cm H₂O±2.0 was measured, while 6 dogs had an average subcapsular pressure of 10.8 cm H₂O±3.0. The subcapsular pressure was found to increase during renal venous constriction and ureteral pressure elevation, procedures which are very likely to lead to a rising renal interstitial pressure.To demonstrate a functional communication between the subcapsular and the deep renal interstitium I¹³¹-labelled albumin was injected into the subcapsular space of 5 rats, while the hilar lymph was collected through a cannulated lymph vessel. It was found that already in the first collection period of 20 min duration a considerable I¹³¹ activity was present in the lymph which consisted mainly of albumin-bound iodide. It is concluded that the low subcapsular pressure is probably valid for the entire renal interstitial compartment.     

Initial cardiovascular response on change of posture from squatting to standing

Summary The immediate cardiovascular responses on active change from the squatting (control) to the standing position differ from those obtained in the lying-to-standing manoeuvre. Without exception, the first beat after changing from squatting to standing showed a decrease in systolic, diastolic and mean pressure by 2.0±1.1 kPa (14.6±8.3 mm Hg), 1.4±1.7 kPa (10.6±12.6 mm Hg) and 1.9±1.0 kPa (13.9±7.3 mm Hg), respectively. During the 4^th or 5^th pulse after standing the pulse pressure was significantly higher than when lying (P<0.01). Mean pressure reached a minimum of 7.7±1.9 kPa (57.8±14.4 mm Hg) after 7.1±1.1s. Thereafter the blood pressure increased to a new level within about 15 s. 11 of 16 subjects demonstrated a biphasic heart rate (HR) response. The maximum HR was reached after 11.0±2.4 s of standing. In all experiments, the peaks in HR were distinctly delayed after the blood pressure clips. We conclude that an arterial baroreflex could be implicated in the immediate HR increase after a squatting-tostanding manoeuvre. The subsequent time course of the initial HR response, however, might be induced by other mechanisms.     

Human cardiovascular reactions to simulated hypovolaemia,modified by the opiate antagonist naloxone

Summary Six healthy males were exposed to 20 mm Hg lower body negative pressure (LBNP) for 8 min followed by 40 mm Hg LBNP for 8 min. Naloxone (0.1 mg·kg^–1) was injected intravenously during a 1 h resting period after which the LBNP protocol was repeated. Systolic, mean, and diastolic arterial blood pressures (SAP, MAP, DAP), and central venous pressure (CVP) were obtained using indwelling catheters. Cardiac output (CO), forearm blood flow (FBF), heart rate (HR), left ventricular ejection time (LVET), and electromechanical systole (EMS) were measured non-invasively. Pulse pressure (PP), stroke volume (SV), total peripheral resistance (TPR), forearm vascular resistance (FVR), systolic ejection rate (SER), pre-ejection period (PEP), PEP/LVET and indices for the systolic time intervals (LVETI, EMSI, PEPI) were calculated. During the second LBNP exposure, only two parameters differed from the pre-injection values: DAP at LBNP=40 mm Hg increased from 60.0±4.8 mm Hg to 64.8±4.1mm Hg (N=4, p<0.02) and LVETI at LBNP=20 mm Hg increased from 384.4±5.2 ms to 396.8±6.2 ms (N=6, p<0.02). In connection with the injection, SAP increased from 128.5±4.2 mm Hg to 134.3±5.4 mm Hg (N=6, p<0.025), PP from 56.5+-2.8 mm Hg to 62.7±3.5 mm Hg (N=6, p<0.01), HR from 54.0±3.1min^–1 to 59.2±4.1 min^–1 (N=6, p<0.01), and LVETI from 407.0±5.6 ms to 413.1±6.0 ms (N=6, p<0.02). This study suggests that endorphins do not have a significant action on the cardiovascular system in the compensated stage of hypovolaemic shock in humans. We found, however, weak evidence that naloxone increases SAP, HR, and LVETI during rest.     

Effect of lower-body positive pressure on postural fluid shifts in men

Summary To quantify the effect of 60 mm Hg lower-body positive pressure (LBPP) on orthostatic blood-volume shifts, the mass densities (±0.1 g· l^–1) of antecubital venous blood and plasma were measured in five men (27–42 years) during combined tilt table/antigravity suit inflation and deflation experiments. The densities of erythrocytes, whole-body blood, and of the shifted fluid were computed and the magnitude of fluid and protein shifts were calculated during head-up tilt (60°) with and without application of LBPP. During 30-min head-up tilt with LBPP, blood density (BD) and plasma density (PD) increased by 1.6±0.3 g · l^–1, and by 0.8±0.2 g · l^–1 (±SD) (N=9), respectively. In the subsequent period of tilt without LBPP, BD and PD increased further to +3.6±0.9 g · l^–1, and to +2.0±0.7 g · l^–1 (N=7) compared to supine control. The density increases in both periods were significant (p<0.05). Erythrocyte density remained unaltered with changes in body position and pressure suit inflation/deflation. Calculated shifted-fluid densities (FD) during tilt with LBPP (1006.0±1.1 g · l^–1,N=9), and for subsequent tilt after deflation (1002.8±4.1 g · l^–1,N=7) were different from each other (p<0.03). The plasma volume decreased by 6.0±1.2% in the tilt-LBPP period, and by an additional 6.4±2.7% of the supine control level in the subsequent postdeflation tilt period. The corresponding blood volume changes were 3.7±0.7% (p<0.01), and 3.5±2.1% (p<0.05), respectively. Thus, about half of the postural hemoconcentration occurring during passive head-up tilt was prevented by application of 60 mm Hg LBPP.H. Hinghofer-Szalkay was a European Space Agency fellow on leave from the Physiological Institute, Karl-Franzens-University, A-8010 Graz, Austria.     

Kinetics of the glomerular ultrafiltration in the rat kidney. An experimental study.

The quantitative relation between the driving forces over the glomerular membrane and the glomerular plasma flow, on the one hand, and the single glomerular filtration rate (SNGFR), on the other, is still uncertain. Micropuncture measurements on Sprague-Dawley rats made it possible to calculate the net driving force over the glomerular membrane. The single glomerular plasma flow was determined from SNGFR and the single nephron filtration fraction (SNFF). The effective plasma flow was measured with PAH for total kidney and for superficial nephrons. The mean glomerular capillary pressure was found to be 62.6 mm Hg. The results indicate a net driving force of about 13 mm Hg at the distal end of the glomerular capillary. SNGFR was found to be 14.1 nl/min-100 g. SNFF amounted to about 0.27. The filtration fractions determined with the PAH method were in the same range. The results indicate a filtration disequilibrium, in contrast to those of Brenner et al. from measurements on a mutant Wistar rat strain. The filtration fractions seemed to be the same in all glomerular populations. It is clear that the SNGFR is pressure dependent. Our earlier findings of a nonautoregulation of the blood flow through the outer glomeruli were also confirmed.