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Biomedical subjects

A E Persson

Publications and source records attributed to A E Persson.

At least 73 records · Page 4Linked to original sources
PubMed1989

Effect of thromboxane inhibition on tubuloglomerular feedback in hydronephrotic kidneys.

The tubuloglomerular feedback (TGF) system is less sensitive after extracellular volume expansion (VE). In rats with partial ureteral obstruction, however, we have previously found increased TGF sensitivity during such expansion. Thromboxane A2 (TXA2) has been reported to be increased in the hydronephrotic kidney, and the present study was undertaken to investigate whether TXA2 might be responsible for these findings. The TGF characteristics were studied, by means of the stop-flow technique, in control and hydronephrotic rats before and after intravenous injection of either a thromboxane synthetase inhibitor or a thromboxane receptor antagonist during hydropenia. After VE, TGF was studied again. Proximal tubular stop-flow pressure (Psf) was measured during perfusion of the loop of Henle with a modified Ringer's solution, the maximal response (delta Psf) to an increased tubular flow rate was determined and the tubular perfusion rate which elicited a half-maximal decrease in Psf, designated the turning point, was recorded. In hydropenic control or hydronephrotic animals, TXA2 did not permanently change the TGF characteristics. During VE of the TXA2-blocked hydronephrotic animals, blocked both with synthetase inhibitor or receptor-antagonist, TGF was reset to a lower sensitivity like VE controls, as indicated by a high turning point and a low delta Psf. It was therefore concluded that thromboxane A2 inhibition does not influence the TGF system in hydropenia, but that the production of thromboxane A2 is responsible for the resetting of the TGF system during VE in hydronephrotic animals.

Animals↗
PubMed1989

Chlorothiazide effect on feedback-mediated control of glomerular filtration rate.

We examined the effect of chlorothiazide (CTZ) on the tubuloglomerular (TG) feedback system in anesthetized Sprague-Dawley rats. During infusion of CTZ (0.25 mg.kg body wt-1.min-1) we found that whole kidney glomerular filtration rate (GFR) decreased by 19% (1.0 +/- 0.1 vs. 0.8 +/- 0.1 ml/min; P less than 0.005). To asses the activity of the TG feedback system during CTZ administration we compared measurements of single-nephron (SN)GFR from tubule fluid sampled separately at proximal and distal sites. During CTZ administration, distally measured SNGFR decreased significantly by 16% (27.3 +/- 1.3 vs. 22.9 +/- 1.1 nl/min; P less than 0.025), whereas proximally measured SNGFR was unchanged. Thus the difference in SNGFR between proximal and distal determination increased during CTZ infusion (4.7 +/- 0.7 vs. 7.7 +/- 0.7 nl/min; P less than 0.025), indicating that CTZ suppresses GFR by TG feedback. Na, K, and Cl concentrations measured in the late proximal tubule fluid during control and CTZ infusions were similar. In early distal tubule fluid samples K and Cl concentrations were unaffected by CTZ infusion, whereas Na concentrations increased by 32% (47.9 +/- 2.7 vs. 63.1 +/- 2.4 mM; P less than 0.001). Proximal tubule microperfusion with 1.0 mM CTZ decreased transport rates of Na and water by approximately 40%, whereas the transport rate of Cl was not affected. In conclusion our results indicate that CTZ reduces GFR by activating TG feedback. The mechanism by which this occurs is in part due to an increase in the strength of the signal.

Absorption↗
PubMed1988

A micropuncture assessment of the effects of contrast media of different osmolality.

The pathophysiology of radiographic contrast media-induced acute renal failure is unclear. Different causes are suggested, including hypertonicity, charged molecules, and toxicity of the media. This study deals with hemodynamic changes after injection of contrast media of high osmolarity iohexol, and metrizoate. Proximal tubular free-flow and stop-flow pressure (Psf), (the latter a marker of glomerular capillary pressure) were measured before, during, and afer injection of contrast media into the renal artery, compared with saline injection, in both normal rats and rats with ureteral obstruction (UO). Urine and electrolyte excretion also were examined. Metrizoate caused an initial decrease in Psf, from 37 to 20 mm Hg, followed by an increase to 81 mm Hg, and the value remained high for 10 minutes. During UO, the elevation of Psf was prolonged. Iohexol injection had a less marked effect. The change in glomerular capillary pressure may be dependent on the osmolarity of the contrast agent.

Animals↗
PubMed1988

Measurements of macula densa cell volume changes in isolated and perfused rabbit cortical thick ascending limb. I. Isosmotic and anisosmotic cell volume changes.

A method to measure time-dependent volume changes in macula densa (MD) cells is described. Cell volume is calculated from cell height measurements for which an image-splitting eyepiece is used. This paper presents the results of experiments designed to investigate the behaviour of the macula densa cells in anisosmotic media, to evaluate the cell volume response to sudden decreases in luminal or peritubular osmolarity and to examine the effect of different luminal NaCl concentrations on the steady-state isosmotic cell volume and on the regulatory volume response to anisosmotic media. The result showed that induced alteration in macula densa cell volume did not change macula densa surface area, but only cell height. The mean control cell height was 13.3 microns +/- 0.4. When MD cells were exposed to a luminal osmolarity of 180 mosM (control 300 mosM) they swelled only to 1.19 +/- 0.02 of the control value and with furosemide present to 1.13 +/- 0.02 or with low NaCl to 1.13 +/- 0.01. While after 5 min of exposure values were 1.15 +/- 0.03, 0.99 +/- 0.02 and 1.02 +/- 0.02, respectively. Addition of furosemide (10(-4) M) to the luminal perfusate (300 mosM) resulted in a rapid decrease in cell height to 0.8 +/- 0.02 in relation to control. When furosemide was removed cell volume was restituted (0.98 +/- 0.03). When luminal perfusate was replaced by mannitol and (12 mM Na+, 7 mM Cl-) cell volume decreased to 0.83 +/- 0.02 of the control value.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Measurements of macula densa cell volume changes in isolated and perfused rabbit cortical thick ascending limb. II. Apical and basolateral cell osmotic water permeabilities.

Cortical thick ascending limbs containing macula densa plaques were dissected and perfused in vitro. Macula densa cell osmotic water permeability of the apical and basolateral membranes were measured by setting up osmotic steps across them in less than 0.1 s and following the ensuing time-dependent cell volume changes. The results of this study are in accordance with the view that the macula densa cells have a relatively low permeability to water. Apical and basolateral osmotic water permeabilities are 2.4 and 30.4 x 10(-4) cm3 s-1 osMolar-1 cm-2 basement membrane area, respectively. No infoldings were taken into consideration. These water permeabilities were not affected by maximal and supramaximal doses of vasopressin. This paper provides new insight into the physiological behaviour of this small, and almost inaccessible, sensing epithelial disc of cells which improves the understanding of its participation in the juxtaglomerular feedback response.

Animals↗
PubMed1988

Back-leak of pelvic urine to the bloodstream.

The aim of the present investigation was to measure the back-leak of pelvic urine to the blood circulation. In normopenic hydronephrotic, dehydrated hydronephrotic and dehydrated control kidneys the back-leak was estimated from a servocontrolled machine which regulated infused saline to keep a present pelvic pressure constant. The disappearance of fluid from the renal pelvis could be measured at different pressure levels, and a pressure-dependent outflow of fluid was found. From these measurements a back-leak conductance could be calculated which proved to be independent of pressure. In the lower pressure range (15-20 mmHg) there was a significantly lower conductance in the dehydrated controls compared with the dyhydrated hydronephrotic kidneys, while in the higher pressure range (25-30 mmHg) no difference was found. From electron microscopical studies the pyelorenal back-leak of fluid in both hydronephrotic and control animals seemed to be most pronounced in the fornix region, as documented by a heavy presence of horseradish peroxidase in the intracellular spaces there. Other experiments with radioactively labelled inulin, which was injected into the pelvic cavity, indicated that most of the back-leak occurred via the renal blood vessels and not through the lymphatic system. The importance of this back-leak was evident from the measurements of the total kidney glomerular filtration rate (GFR) at a slightly increased pelvic pressure, where some of the urine with radioactive tracer flows back to circulation. The back-leak of pelvic urine could also affect the concentration mechanism by removing diluted urine which had flowed over the renal papilla, and through water and urea diffusion increased papillary interstitial osmolarity.

Animals↗
PubMed1988

Pressure and flow measurements in the partially obstructed ureter of the rat.

Hydronephrosis in man or experimental animals can be caused by an increased ureteral flow resistance. This condition can in the long run prove harmful to renal function. We compared two ways of measuring ureteral flow resistance in animals with and without a ureteral hindrance, the hindrance being induced by embedding the ureter in the psoas muscle. One needle connected via catheters to a pressure recording system and another connected to a pump system were introduced through the parenchyma into the renal pelvis. Experiments were carried out with two procedures: 1) infusion of 0.5 ml x min-1 of saline into the renal pelvis was performed while recording the pressure response; 2) a servocontrolled pump system was used which regulated the flow introduced into the renal pelvis to keep a preset pressure at a constant level. In the first group of experiments we did not establish a steady-state pressure despite 20-30 min of infusion. The result from the second series of experiments indicated that steady-state flow measurements could be achieved at the different pressure levels between zero and 30 mmHg. A good linear relationship between pressure and flow was found, even though a considerable hysteresis was observed. Furthermore, a reduced flow resistance down to a certain level at increased pressure was also recorded. As expected, the resistance to flow was significantly lower in the control than in the hydronephrotic animals. In order to investigate the diagnostic ability of the linear relationship between pressure and flow, prediction regions for one future animal were calculated. It seemed possible that determination of the whole pressure-flow relationship in the pressure range between zero and 30 mmHg will prove useful to determine the flow hindrance in hydronephrotic animals.

Animals↗
PubMed1988

Renal abnormalities in experimental models of hypertension: the SHR versus the Milan HR.

Renal regulation of extracellular fluid volumes via the tubuloglomerular feedback control (TGF) has been studied in rat experiments. Important modulation of the TGF mechanism was achieved from arterial blood pressure level and extracellular fluid volume via renal interstitial pressure changes. This volume-regulating mechanism has been studied in spontaneously hypertensive rats of the Milan strain (MHS) and compared with Milan normotensive rats (MNS). During development of hypertension, the TGF mechanism was highly sensitive and activated to reduce glomerular filtration rate and retain electrolytes and water. When blood pressure was increased in the adult MHS animals the TGF mechanism was normalized. It could be speculated that the cause of the increased TGF mechanism was dependent on an increased Na-K-2 Cl cotransport into the macula densa cells. In SHR rats compared to Wistar-Kyoto rats, the TGF sensitivity was also increased but, in contrast, the TGF mechanism was not activated in these animals to retain fluid. Some other mechanism for the development of hypertension in these rats has to be proposed.

Animals↗
PubMed1987

Tubuloglomerular feedback in animals with unilateral, partial ureteral occlusion.

Previous experiments have shown that the sensitivity of the tubuloglomerular feedback system (TGF) is reduced by volume expansion in normal rats. This reduction in sensitivity is probably mediated by changes in the renal interstitial pressure. The present study was designed to investigate the TGF control system during volume expansion in rats with chronic, partial ureteral occlusion--hydronephrosis. Hydronephrosis was induced on the left or right side according to the method described by Ulm and Miller, in weanling Sprague-Dawley rats three weeks old. Three to six weeks later the rats were prepared for whole kidney and micropuncture experiments. Sham-operated animals were used as controls. Net interstitial pressure (that is, interstitial hydrostatic pressure minus interstitial oncotic pressure) was higher in the hydronephrotic, volume expanded animals than in the volume expanded controls. From findings in earlier investigations this increase in interstitial pressure would have been expected to reduce TGF sensitivity but this sensitivity was increased in the hydronephrotic kidneys, as indicated by a reduction in the turning point, the tubular flow rate at which 50% of the maximal stop-flow pressure response was observed (14.4 nl/min, sham-operated control 33.4 nl/min). Strong activity of the TGF mechanism was also indicated by a large proximal-distal difference in the single-nephron glomerular filtration rate (11.9 nl/min versus 3.3 nl/min in sham-operated controls) in the hydronephrotic kidney during volume expansion. Thus, in hydronephrotic kidneys in the latter condition the TGF mechanism was highly sensitive and activated to reduce the glomerular filtration rate. This mechanism may protect the diseased kidney from high intrapelvic pressures which otherwise could damage the kidney during saline volume expansion.

Animals↗
PubMed1986

Influence of water-diuresis or saline volume expansion on deep nephron tubuloglomerular feedback.

We have recently demonstrated the existence of a tubuloglomerular feedback mechanism in juxtamedullary nephrons in rat kidneys during antidiuresis. In the present experiments, we have investigated the influence of water-diuresis on Munich Wistar rats and in homozygote Brattleboro rats. We have also observed the effect of saline volume expansion on the tubuloglomerular feedback of juxtamedullary nephrons in Munich Wistar rats. For comparison, the feedback mechanism was also studied in surface nephrons during water-diuresis in Munich Wistar rats. Measurements of flow rate in the descending limb of Henle and single nephron glomerular filtration rate (GFR) using micropuncture at the renal papilla were performed, while the ascending limb was microperfused at varying perfusion rates with a modified Ringer solution. In surface nephrons early proximal flow rate, single nephron GFR and stop-flow pressure was measured during microperfusion of the end-proximal loop. No significant changes were measured in surface nephrons during water-diuresis: the tubular flow rates, feedback responses, stop-flow pressure and stop-flow pressure changes were similar to those during anti-diuresis. In juxtamedullary nephrons, Henle loop flow rate increases during water-diuresis but the feedback-mediated flow and single nephron GFR response curves obtained during microperfusion were unaltered compared to controls. Together, these results indicate that the feedback could be more activated during water-diuresis than during control conditions. On the other hand, during saline volume expansion, reduced tubuloglomerular feedback sensitivity was found as shown earlier for surface nephrons. The reduction of tubuloglomerular feedback sensitivity therefore seems to be important in maintaining salt-, but not water-balance.

Animals↗
PubMed1986

Increased tubuloglomerular feedback activity in Milan hypertensive rats.

Studies of whole-kidney function and micropuncture measurements in superficial nephrons were performed to investigate the role of the tubuloglomerular feedback (TGF) in the excretion of salt and water in hydropenic and volume-expanded rats of the spontaneously hypertensive Milan strain (MHS). The rats were 3.5-5 and 5-7 wk old, and age-matched animals from the Milan normotensive strain (MNS) served as controls. There was no difference in mean arterial blood pressure (Pa) between the 3.5- to 5-wk-old prehypertensive MHS (MHSp) and MNS rats, but the glomerular filtration rate (GFR) was higher in MHSp than in MNS [1.35 vs. 0.80 ml X min-1 X g kidney wt (KW)-1, P less than 0.01]. The distal single-nephron glomerular filtration rate (SNGFR) was also higher in MHSp than in MNS (28.6 vs. 20.2 nl X min-1 X g KW-1, P less than 0.05). TGF was determined from both stop-flow pressure response and proximal and distal SNGFR. It was found that MHSp exhibited essentially no TGF response. During development of hypertension 5- to 7-wk-old MHS (MHSd) had a higher Pa than MNS (120 vs. 98 mmHg, P less than 0.01). Normally GFR and SNGFR increase with age, and such was the case with MNS (0.8 to 1.02 ml X min-1 X g KW-1 and 20.2 to 23.4 nl X min-1 X g KW-1), but in MHSd there was a decrease in both GFR and SNGFR with age (1.35 to 1.10 ml X min-1 X g KW-1 and 28.3 to 18.3 nl X min-1 X g KW-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

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)

Animals↗
PubMed1985

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.

Animals↗
PubMed1985

Tubuloglomerular feedback during elevated renal venous pressure.

Interstitial hydrostatic and oncotic pressures are believed to influence the sensitivity of the tubuloglomerular feedback (TGF) control. To further investigate this hypothesis, three groups of experiments with elevated renal venous pressure (Prv) were conducted. We investigated 1) the stop-flow pressure (Psf) feedback response; 2) urine flow rate, glomerular filtration rate (GFR), subcapsular interstitial hydrostatic pressure (Psc), and interstitial oncotic pressure (pi int); and 3) the proximal-distal single nephron glomerular filtration rate (SNGFR). The results showed that the Psf feedback response was unaffected by Prv elevation. Psc increased from 0.5 to 3.5 mmHg and pi int increased from 2.1 to 5.8 mmHg; thus, no change in net interstitial pressure (Psc - pi int) was found during elevated Prv. There was a significant proximal-distal SNGFR difference during both control and elevated Prv (8.0 and 6.3 nl/min, respectively). A 20% reduction in total GFR and SNGFR was observed at increased Prv. In separate experiments using the same protocol, a 5% body wt/h volume expansion with saline was induced before Prv was elevated. During volume expansion, TGF sensitivity declined and net interstitial pressure increased, both of which were normalized by increasing Prv. The results show that the TGF sensitivity is normal during elevated Prv to 20 mmHg and that the increase in Psc during this condition is counter-balanced by an increase in pi int. In addition, the decrease in GFR and SNGFR during increased Prv cannot be explained by a change in TGF activity. However, these findings indicate that both interstitial hydrostatic and oncotic pressures may influence the resetting of the TGF sensitivity.

Animals↗
PubMed1985

Partial ureteric obstruction in weanling rats. I. Long-term effects on the renal morphology.

Partial obstruction of one ureter was created in weanling rats (3 weeks old) and its effects were studied after 3, 6, and 9 weeks. Within 3 weeks, a considerable hydronephrosis had appeared, which did not progress with time. No effect on parenchymal weight was observed, either on the obstructed side or on the contralateral, intact one. Histological examination revealed a marked deformation of the papilla in about 25% of the hydronephrotic kidneys and evidence of chronic pyelonephritis in 40%. However, the inflammatory changes were restricted to the attenuated circumhilar 'edges' of the parenchyma, thus involving only a minor portion of the kidney. The body weight of the animals obstructed for 9 weeks was 12% lower than that of normal, sham-operated controls. In summary, the effect on the renal parenchyma of partial ureteric obstruction, created in the weanling period, was relatively discrete and less pronounced than when obstruction is performed in the neonatal period.

Animals↗
PubMed1985

Arterial hypertension--a disease of the juxtaglomerular apparatus?

From a special strain of genetically hypertensive rats, the Milan hypertensive strain (MHS), arterial hypertension can be transplanted with the kidney to the Milan normotensive strain (MNS). During development of hypertension in MHS rats there was an activation of the tubuloglomerular feedback control that reduced glomerular filtration rate, leading to retention of electrolytes and fluid. This increased extracellular fluid volume reduces feedback sensitivity, but in a fashion that gives rise to chronic extracellular fluid expansion and can thereby raise the blood pressure. In a limited sense, arterial hypertension in these animals exists to prevent the kidney from retaining more extracellular fluid volume. The altered function in the juxtaglomerular apparatus of the MHS rats thus may explain the rise in arterial blood pressure.

Animals↗
PubMed1985

Renal vasodilation after unilateral renal ablation.

Renal blood flow was studied in rats 120 minutes after unilateral renal ablation. The influence of endogenous prostaglandin formation was evaluated by indomethacin treatment prior to the ablation. Radioactive microspheres were used for estimation of the total renal and cortical blood flow, and the renal medullary blood flow was determined with the 86-Rb chloride extraction method. The total blood flow in the remaining kidney was increased by 80% following contralateral ablation, with augmentation in all areas, particularly in the deep medullary region. Indomethacin treatment in intact rats evoked increased blood flow as compared with the indomethacin control group. The results indicated that the renal blood vessels respond to ablation of the contralateral kidney with dilation in all kidney regions, and that this vascular dilation may be prostaglandin-mediated.

Animals↗