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Biomedical subjects

A E Persson

Publications and source records attributed to A E Persson.

At least 91 records · Page 5Linked to original sources
PubMed1985

Tubuloglomerular feedback response in the contralateral kidney after 24-hour unilateral ureteral obstruction.

Reduction of the functioning renal mass by unilateral nephrectomy or unilateral ureteral occlusion (UUO) leads to increased function of the remaining nephrons, an important factor being the glomerular filtration rate (GFR). GFR can be modified via the tubuloglomerular feedback control (TGF), which senses the distal delivery of fluid and alters the tonus of the glomerular arterioles. The aim of the present study was to investigate the TGF sensitivity in the intact left kidney of rats after 24 hours of right ureteral occlusion. Using a micropuncture technique, proximal tubular stop-flow pressure (Psf), as a relative index of glomerular capillary pressure, was measured upstream to the block, while late proximal segments were perfused with Ringer solution (rates 0-40 nl/min). The maximal drop in Psf and the tubular flow rate at which 50% of this response was achieved, the turning point (TP), were determined. Considerable decrease in the sensitivity of the TGF system in the contralateral kidney during UUO was indicated by a significantly higher TP as compared with control rats (sham operation), viz. 29 v. 19 nl/min. Maximal Psf drop after UUO was significantly less than in the controls (6 v. 12 mm Hg). Reduced TGF sensitivity in the contralateral kidney after protracted UUO is a prerequisite for that kidney's increased excretion of salt and water to compensate for the loss of functioning renal mass.

Adaptation, Physiological↗
PubMed1984

Tubuloglomerular feedback and interstitial pressure in obstructive nephropathy.

The possible role of the tubuloglomerular feedback (TGF) mechanism in the altered glomerular hemodynamics and tubular reabsorption which occur with prolonged (24-hr) ureteral obstruction and the changes in renal interstitial hydrostatic and oncotic pressure which may modulate TGF sensitivity were examined. The proximal tubule stop-flow pressure (PSF) response to increased distal tubular flow rates (TGF activity) was determined in rats with sham operation, 24-hr unilateral ureteral obstruction (UUO), or 24-hr bilateral ureteral obstruction (BUO), both before and for 2 hr after relief of obstruction. Subcapsular hydrostatic pressure, lymph flow and oncotic pressure, clearance and excretory data were measured in the second series of animals. During and after release of UUO, TGF sensitivity was increased, as indicated by the marked decrease in the loop perfusion rate at which 50% of the maximum decrease in PSF occurred (the turning point of TGF activation). Interstitial oncotic pressure but not hydrostatic pressure was significantly increased in UUO kidneys. In BUO rats, the turning point for TGF activation was slightly higher than the controls and the change in PSF with maximum loop perfusion rates was reduced, indicating a blunting of the TGF response before and particularly during postobstructive diuresis after release of BUO. Interstitial hydrostatic and oncotic pressures were both slightly increased resulting in no changes in net interstitial Starling forces. We conclude that enhanced TGF sensitivity after release of prolonged UUO, associated with increased interstitial oncotic pressure, may play a role in preventing postobstructive diuresis, while the blunting of TGF sensitivity after BUO may contribute to this phenomenon.

Animals↗
PubMed1984

Total and regional renal blood flow during complete unilateral ureteral obstruction.

Regional renal blood flow was investigated after 1, 2, 12 and 24 h of unilateral ureteral obstruction in rats. Total renal and cortical blood flow rates were determined by the microsphere technique and regional medullary blood flow by the 86-Rb extraction method. The kidneys were microdissected into cortex and medulla, which was further divided into the outer stripe and the inner stripe of the outer zone, and the inner zone. In the obstructed kidneys cortical blood flow increased by 33% after 1 h of obstruction, but was normalized after 2 h. After 12 and 24 h this flow was significantly decreased (55% and 65% of control respectively). The pattern of total renal blood flow was similar to that of cortical blood flow. In the outer stripe there was an initial increase (44%) after 1 h, but later no significant deviations from control values were found. After 1 h of obstruction the blood flows in the inner stripe and the inner zone were not significantly different from control values. A significantly decreased blood flow was seen in the inner stripe after 2 h (57% of control) and in the inner zone after 12 h (58% of control). A significant recovery of the blood flow had occurred in the inner stripe and the inner zone after 24 h of obstruction. In the contralateral, non-obstructed kidney no significant changes were found, besides an increased innerstripe blood flow after 24 h of UUO.

Animals↗
PubMed1984

The effect of 2 hours of complete unilateral ureteral obstruction on tubuloglomerular feedback control.

The mechanisms affecting renal blood flow and filtration during and after unilateral ureteral obstruction (UUO) are incompletely understood. Since ureteral obstruction leads to changes in interstitial pressure and volume, and since we have previously shown that interstitial pressure conditions can modulate the sensitivity of the tubuloglomerular feedback (TGF) control system, we sought in the present study to define the contribution of the TGF system to changes in GFR during and after UUO, and to observe associated changes in pressures in vessels, tubules and the interstitial space. Interstitial pressures and glomerular filtration rate (GFR) were measured in one group of Sprague Dawley rats. Interstitial hydraulic pressure was determined with a thin catheter placed in the subcapsular space. Interstitial oncotic pressure was estimated from the protein concentration in collected hilar lymph. In a second group of rats proximal tubule pressure (PT) and stop-flow pressure (PSF) were measured during the first three hours of UUO and after 24 h UUO. In a third group of rats PSF was measured while the loop of Henle was perfused at different rates. The sensitivity of the TGF system was determined from the maximal drop in stop-flow pressure (delta PSF) and the turning point (TP)--the tubule perfusion rate at which 50% of this maximal stop-flow pressure response was obtained. In a fourth group of rats proximal tubule flow-rate was measured after release of 2 hrs UUO. The results show that PT and PSF are both increased during the first three hours of obstruction and that they return to normal or sub-normal levels after 24 h of UUO.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

The effect of intraarterial infusion of prostacyclin on the tubuloglomerular feedback control in the rat.

Effects of intraarterial prostacyclin (PGI2) infusions on interstitial hydrostatic and oncotic pressures and on the tubuloglomerular feedback (TGF) control of glomerular filtration rate (GFR) were studied in rat kidneys. The hilar lymph flow rate was used as a measure of interstitial hydrostatic pressure and the lymph protein concentration was used for interstitial oncotic pressure estimation. In the micropuncture experiments the stop-flow pressure technique was employed for determining the TGF characteristics, i.e. stop-flow pressure (PSF), maximal reduction of PSF (delta PSF) and turning point (TP), defined as the end-proximal flow rate at which 50% of delta PSF was obtained. Non-hypotensive doses of PGI2 (50 to 100 ng X kg-1 B.W. X min-1) infused in 30 min evoked an increase in urine and lymph flow rates and a decrease in lymph protein concentration, but did not affect GFR. delta PSF was reduced (9.9 +/- 1.0 mmHg versus 4.7 +/- 2.2 mmHg) and TP increased (22 +/- 2 nl/min versus 34 +/- 2 nl/min), but the PSF was unaffected. These changes were seen during the infusion period and during the immediate post-infusion control period of 30 min. Our data indicate that non-hypotensive doses of PGI2 in some way can affect the renal interstitial pressure and the TGF control system.

Animals↗
PubMed1984

Feedback pressure-flow responses in normal and angiotensin-prostaglandin-blocked rats.

We have examined the response of directly and indirectly (stop-flow) measured glomerular capillary hydrostatic pressure (PGC) and single nephron glomerular filtration rate (SNGFR) to increases in late proximal tubular flow rate in hydropenic rats and rats in which angiotensin II (ANG II) and prostaglandin generation was reduced by 3- to 5-day pretreatment with converting enzyme inhibitor (MK-421) and meclofenamate. In control rats, PGC (48 +/- 2 mmHg) decreased 9 +/- 1 mmHg when 25 nl/min was added to late proximal flow in unobstructed tubules, and PGC decreased 9 +/- 1 mmHg when late proximal perfusion rate was increased from 0 to 40 nl/min, incrementally, in wax-blocked tubules. The turning point or half-maximal response for PGC was at perfusion rates of 23 +/- 2 nl/min. Stop-flow estimated PGC (47 +/- 1 mmHg = control) responses were nearly identical. SNGFR decreased from 30 +/- 1 to 21 +/- 1 nl/min with increased perfusion in control rats. In ANG II-prostaglandin-blocked rats, PGC and stop-flow pressure responses were completely eliminated, yet SNGFR response persisted (36.2 to 28.0 nl/min) but to a somewhat lesser extent. Both direct and indirect PGC decrease with increases in late proximal flow rate in untreated rats. Studies in ANG II-prostaglandin-blocked rats suggest that tubuloglomerular feedback SNGFR responses can occur without changes in PGC, possibly via parallel changes in afferent and efferent arteriolar resistances.

Angiotensin I↗
PubMed1983

Effect of renal tubular obstruction on stop-flow pressure and glomerular deposition of fibrin during intravascular coagulation in the rat.

Intravascular coagulation in the rat kidney was induced by intravenous infusion of thrombin for 1 hr. The proximal tubular free-flow (Pt) and stop-flow (Psf) pressures were measured by micropuncture. Some proximal tubules were obstructed with solid paraffin before infusion of thrombin. In certain rats saralasin or indomethacin was administered for 1 hr starting 30 min after the thrombin infusion, and the effect on the tubular pressures was studied. The deposition of fibrin in the glomeruli was examined by light and electron microscopy. Pt fell from 15 +/- 1 (SE) to 7 +/- 2 mm Hg (P less than 0.05) during the infusion of thrombin. After a brief period of increased pressure the Psf fell rapidly from 37 +/- 1 to 17 +/- 1 mm Hg (P less than 0.05). In the previously obstructed nephrons the pressure (Po) increased parallel to the increase in Psf but remained elevated after the infusion of thrombin, 54 +/- 2 mm Hg. The arterial blood pressure (Pa) increased from 119 +/- 2 to 138 +/- 3 mm Hg (P less than 0.05). Saralasin raised the Psf from 15 +/- 1 to 19 +/- 1 mm Hg (P less than 0.05) but had no effect on Pt, Po, or Pa. Indomethacin did not influence the pressures. Morphological examination revealed fibrin in all glomeruli of normal nephrons. In the previously obstructed nephrons the deposition of fibrin was almost totally prevented. The results suggest that glomerular filtration is important for deposition of fibrin in the kidney.

Animals↗
PubMed1983

Modulation of renal tubular function by renal interstitium.

Rat micropuncture experiments have been performed to investigate the influence of renal interstitial pressure conditions on proximal tubular fluid absorption and on the tubulo-glomerular feedback mechanism. The feedback mechanism works by sensing the distal tubular fluid flow rate at the macula densa segment and adjusting the tonus of the arterioles with resulting changes in blood flow and glomerular filtration rate. It was found that in situations with high hydrostatic and low oncotic pressure within the interstitium like in saline volume expansion and post-nephrectomy situations, proximal tubular fluid absorption and the sensitivity of the tubulo-glomerular feedback control are reduced giving rise to increased urine production without activating the feedback mechanism. In situations with low hydrostatic and high oncotic interstitial pressures like in dehydration, hypotension and hypovolemia proximal fluid absorption and feedback sensitivity is increased, feedback sensitivity even so much that the mechanism is activated to reduce GFR even though the load to the distal portion of the nephron is reduced below normal. In this way renal interstitial pressure-volume conditions can modulate renal function in response to extracellular fluid needs and blood pressure level.

Absorption↗
PubMed1983

Acidification in the distal tubule of the Amphiuma kidney.

The acidification of the urine within the distal tubule of Amphiuma means was studied with micropuncture techniques. Antimony microelectrodes calibrated in vivo were used for measuring the intratubular pH and samples were taken for the determination of Na+- and Cl- -concentrations and for determining buffer lines within the HCO-3-CO2 buffer system. The TF/P Na+ was used as a relative length determinator and a significant acidification along the length of the tubule was found. The pH in the tubule was more acid than samples equilibrated at blood PCO2. This disequilibrium can be described in terms of an imbalance within the Henderson-Hasselbach formula or/and as a PCO2-gradient across the tubular wall. The calculated PCO2-gradient was found to be correlated to the arterial PCO2 and the acidification to the arterial pH. The greatest pH-gradient is generated in the collecting duct and in the bladder.

Acid-Base Equilibrium↗
PubMed1983

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 decreased 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.

Animals↗
PubMed1983

Activation of the tubuloglomerular feedback mechanism in dehydrated rats.

To study the influence of the tubuloglomerular feedback control (TGF) on the regulation of glomerular filtration rate (GFR) during dehydration, micropuncture experiments were performed on surface nephrons of dehydrated rats. Dehydration was achieved by withdrawal of food and water for 24 h. The urine flow rate decreased to 1.5 microliters/min (controls 2.9 microliters/min) and GFR decreased in these rats to 0.80 ml/min (controls 1.22). TGF was studied by two different micropuncture procedures. With the first technique the changes in proximal stop-flow pressure in response to changes of the late proximal microperfusion rate were measured. With this technique the perfusion rate necessary to induce a half maximal stop-flow pressure response, the turning point, was also determined. An increased TGF sensitivity was found in dehydrated rats, as indicated by increased stop-flow pressure responses (35 versus 26%) and decreased turning points (16 versus 21 nl/min). With the second micropuncture technique the single nephron GFR (SNGFR) was measured at distal and proximal tubular sites, in the same nephron. Distal SNGFR was decreased during dehydration to 32.2 nl/min, versus 42.7 nl/min in controls. A significant difference between paired SNGFR measurements in the same nephron was observed during dehydration, the proximal value being 5.3 nl/min higher than the distal, whereas this difference was not seen in control rats. This finding indicates that activation of the feedback mechanism takes place to reduce SNGFR. It is concluded that the decrease in whole kidney GFR is partly caused by the observed increase in feedback activity. The present results are also in agreement with our earlier hypothesis that the hydrostatic and oncotic pressure conditions within the interstitial space surrounding the macula densa cells modulate the sensitivity of the tubuloglomerular feedback mechanism.

Animals↗
PubMed1983

The effect of tubular perfusion with PGE2, PGF2 alpha, and PGI2 on the tubuloglomerular feedback control in the rat.

The prostaglandins (PG) of the renal medulla might affect the nephron and the cortical arteriolar function via the tubular route. To investigate this question PGE2 (1 microgram/mL), PGF2 alpha (10 micrograms/mL), or PGI2 (1 ng/mL) was added to the tubular perfusion solution when the characteristics of the tubuloglomerular feedback (TGF) control were measured. The experiments were performed on Sprague-Dawley rats. The proximal tubular stop-flow pressure (PSF) was measured upstream to a wax block, while at the same time the distal nephron was perfused with prostaglandin-containing or prostaglandin-free solutions at different flow rates varying from 0 to 50 nL/min. The maximal drop in PSF (delta PSF) and the tubular flow rate at which 50% of the delta PSF response was obtained, the turning point (TP), were determined. When PGE2 or PGF2 alpha was added to the tubular perfusion solution in the control animals a significant increase in feedback sensitivity was found. After 10 min of tubular PGI2 perfusion the feedback sensitivity was almost completely abolished, with a delta PSF of 0.8 mmHg (1 mmHg = 133.322 Pa) (control 8.4 mmHg) and a TP of greater than 40 nL/min (control 22 nL/min). After nephrectomy the feedback sensitivity was reduced, with a delta PSF of 2.0 mmHg and a TP of greater than 40 nL/min. When PGE2 was added to the tubular perfusion solution in the uninephrectomized animals, the feedback sensitivity was increased to the control level, with a delta PSF of 8.2 mmHg and a TP of 20.0 nL/min.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Evidence for tubuloglomerular feedback in juxtamedullary nephrons of young rats.

To determine whether the filtration rate of juxtamedullary nephrons is regulated by tubuloglomerular feedback (TGF), we developed two micropuncture techniques suitable for the papilla of young rats. One consisted of measuring the tubular flow in descending limbs of Henle loops (VDLH) while the ascending limbs of the loop of Henle (ALH) were perfused at various rates with three different solutions: modified Ringer, artificial Henle loop solution, and Ringer containing 10(-4) M furosemide. SNGFR was also measured in several juxtamedullary nephrons. The other protocol consisted of measuring the tubular stop-flow pressure (PSF) in descending limbs of the loop of Henle upstream to a wax block. Distal to the block Ringer was perfused at various rates through ALH. Our results provide the first evidence of a TGF response in juxtamedullary nephrons. VDLH and SNGFR decreased during Ringer perfusion to 42 +/- 4 and 44 +/- 4% of their values at zero perfusion. The same pattern was observed using Henle loop solution as perfusate, whereas with furosemide VDLH did not change. The maximal decrease in PSF was 14.1 +/- 1.4 mmHg. The perfusion rate necessary to induce a half-maximal PSF decrease was 9.1 +/- 0.9 nl/min. Similar micropuncture techniques were used in proximal tubules of surface nephrons in these rats, which in comparison to the deep nephrons showed smaller feedback responses. The mechanism seems to be active at physiological nephron flow rates in both nephron populations. Thus, TGF can exert its effect on GFR of the whole kidney by acting in both deep and surface nephrons.

Animals↗
PubMed1983

Renal tubular secretion of piretanide and its effects on electrolyte reabsorption and tubuloglomerular feedback mechanism.

Piretanide [HOE 118; 4-phenoxy-3-(1-pyrrolidinyl)-5-sulfamoxylbenzoic acid] is a new diuretic with a saluretic effect similar to that of furosemide. The present experiments were undertaken to investigate if transport of piretanide into the tubular lumen determines the diuretic response and what effect piretanide has on the tubuloglomerular feedback control and loop of Henle electrolyte transport. To study the first question, five healthy subjects were investigated. Piretanide, inulin and p-aminohippuric acid were continuously infused. After equilibration, 1 g of probenecid was given which reduced the tubular secretion of piretanide to one-sixth of control level. The reduction in diuresis was 41.4% while it was 59.5, 63.9 and 45.8% for the urinary excretion of chloride, sodium and potassium, respectively. In a second series of experiments in rats a proximal tubular stop-flow pressure response at increased distal delivery of fluid was measured when Ringer's solution, Ringer's solution plus furosemide (10(-4) M) or bumetanide (5 X 10(-5) M) or piretanide (10(-4) M and 5 X 10(-5) M) was added to the tubular perfusion solution. The results indicate that the feedback could be completely blocked by any of these diuretics. The fluid absorption in the loop of Henle was studied in separate experiments and the addition of piretanide (10(-4) M) greatly reduced chloride and absolute fluid absorption from this nephron segment. The present results indicate that tubular secretion of piretanide is important for the diuretic response and that piretanide inhibits the fluid absorption in the loop of Henle and the tubuloglomerular feedback control which would otherwise blunt the diuretic response with a reduction in glomerular filtration rate.

Diuretics↗
PubMed1982

The effect of indomethacin on glomerular capillary pressure and pelvic pressure during ureteral obstruction.

The present investigation was undertaken to determine whether elevated glomerular capillary and pelvic pressure resulting from ureteral obstruction could be lowered by injection of indomethacin. In hydropenic rats and rats subjected to saline volume expansion, the mean arterial blood pressure, renal pelvic pressure and proximal tubular free flow and stop-flow pressures were measured during acute ureteral obstruction. Indomethacin was injected intravenously 30 to 45 minutes after obstruction at a renal pelvic pressure of 35 mm. Hg or higher. In the former group of rats the proximal tubular stop-flow pressure decreased by an average of 32 per cent and renal pelvic pressure by 27 per cent on administration of indomethacin, whereas in the volume expanded rats (saline, 2 per cent of body weight) these pressures did not change significantly. These results suggest that the vasodilation consequent to ureteral obstruction in hydropenic animals is caused by prostaglandins release and can be abolished by indomethacin, whereas the vasodilation that results from ureteral obstruction in volume expanded animals may be affected by additional mechanisms.

Adult↗