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M Sjöquist

Publications and source records attributed to M Sjöquist.

48 records · Page 3Linked to original sources
PubMed1985

Experimental obstructive hydronephrosis in newborn rats. VI. Long-term effects on glomerular filtration and distribution.

Partial obstruction of one ureter was created in newborn rats and its effects were studied after the rats matured. The obstructed pelvis was found to be considerably enlarged. The parenchymal weight was 19 per cent lower and the whole kidney glomerular filtration rate was 43 per cent lower than on the contralateral intact side (p less than 0.001); however, these figures probably include a compensatory increase on the intact side. In the central part of the cortex, the glomerular filtration rate/mg. cortex was 21 per cent lower in the hydronephrotic kidney (p less than 0.02), but there was no intracortical redistribution. The glomerular density in this region was 24 per cent higher on the hydronephrotic side (p less than 0.001), because the glomeruli were crammed together in the distended cortex. No redistribution of glomeruli was found. The results are discussed and compared with previous findings from our laboratory. In this model, partially obstructive uropathy was found to cause only a moderate depression, but no redistribution, of the filtration.

Animals↗
PubMed1985

The effect of a converting enzyme inhibitor on autoregulation and intrarenal distribution of glomerular filtration in the rat.

The role of the renin-angiotensin system in the autoregulation and distribution of the single nephron glomerular filtration rate (SNGFR) in anaesthetized, normotensive rats was investigated. SNGFR in outer cortical (OC) and inner cortical (IC) nephrons of the left kidney were measured with a modified Hanssen technique at three levels of renal arterial pressure (RAP): at a spontaneous arterial pressure; at a value within the autoregulatory limit, 100 mmHg; and at the lower limit of the autoregulatory range, 70 mmHg. This was done in control rats and in rats given a continuous i.v. infusion of the converting enzyme inhibitor (CEI) captopril (3 mg . h-1 X kg-1 BW). In control rats there was complete autoregulation of SNGFR in both OC and IC nephrons when RAP was reduced to 100 mmHg. Further reduction to 70 mmHg elicited different responses among the cortical layers, associated with a decrease in SNGFR. A fractional redistribution of glomerular filtration rate towards IC nephrons was evident. Administration of CEI at spontaneous RAP increased SNGFR in IC nephrons compared with values in control rats, but did not notably alter SNGFR in OC nephrons. Reduction of RAP to 100 mmHg during CEI infusion caused SNGFR to decrease below control values in both OC and IC nephrons, and the autoregulation as found in control rats was impaired. When RAP was lowered to 70 mmHg during CEI administration there was a progressive decrease in SNGFR in all cortical layers, although absolute changes were much greater in IC nephrons than in OC nephrons.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1985

Time-dependent heterogeneity of filtration rate in the autoregulating rat kidney.

Experiments were performed to study the regulation of the single-nephron glomerular filtration rate (SNGFR) in superficial and juxtamedullary nephrons, as the left kidney of Sprague Dawley rats was submitted to a reduced arterial pressure of 70 mmHg by means of an aortic clamp. The SNGFR at different cortical levels was measured 0.5, 1, 5, 20 or 45 min after the reduction, in order to ascertain whether the effects of the regulatory mechanisms are modified with time. A Hanssen technique was used, which allows one determination of filtration rates per animal. At a renal arterial pressure (RAP) of 100 mmHg (= control animals) the SNGFR amounted to 20 +/- 1.2 and 23 +/- 0.8 nl X min-1 X g-1 kidney weight in the outer and inner cortical (OC, IC) nephrons. When RAP was further reduced to 70 mmHg, the autoregulation of SNGFR, determined after 0.5 min, was highly efficient for both OC and IC nephrons (19 +/- 2.0, 23 +/- 2.6). A prolonged reduction in RAP caused a gradual decline in SNGFR. The filtration rate measured after 5 min was 15 +/- 1.4 for OC and 20 +/- 1.8 for IC nephrons. The decline was most pronounced for OC nephrons, which led to a fractional redistribution in favour of IC nephrons. Thus, SNGFRIC/SNGFROC was 1.16 +/- 0.065 when RAP was 100 mmHg and 1.41 +/- 0.126 after 5 min with an RAP of 70 mmHg. It is well documented that suprarenal aortic occlusion is a powerful stimulus for the release of renin. This was manifested as an increase in the arterial pressure proximal to the aortic clamp.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

A method for in situ measurement of ionic concentration in picoliter samples of renal tubular fluid.

A method permitting rapid and frequent determination of the total ionic concentration in renal tubular fluid samples, by measuring sample electrical impedance, is described. No special electrodes or sophisticated equipment are required. Since picoliter volumes are sufficient for measurement, tubular fluid dynamics are not significantly disturbed by the sampling procedure. The sample is aspirated into the tip of the standard glass micropipette and its ionic concentration, in the range of 100-1000 mmol/l, can be determined by any sensitive impedance-measuring device. In the present studies the Wheatstone bridge of the Wiederhielm apparatus for pressure measurement in micropuncture studies was used for the purpose. The obvious limitation of the method is that the measurements do not include non-electrolytes and cannot differentiate between individual ion species.

Animals↗
PubMed1984

Renal interstitial volume of the rat kidney.

The intravascular plasma volume and the interstitial volume of the rat kidney were determined by an indicator dilution method with a bolus injection of 125-I-labelled human serum albumin and 51-Cr-EDTA into the renal artery and subsequent recording of the indicator-dilution curves in the venous effluent, sampled at intervals of 0.33 s. The curves allowed determination of both the mean transit time of the two indicators and total renal plasma flow. The volumes of distribution were obtained by multiplying these two factors. Under control conditions the plasma volume was 93.0 +/- 11.2 microliters/100 g rat (mean +/- SE), which is 17.9% of the total kidney volume. The interstitial volume was 68.3 +/- 8.6 microliters/100 g, corresponding to 13.1% of the total kidney volume. During expansion with 0.15 M NaCl, 10% of body weight, the plasma and interstitial volumes were not significantly increased. The values for the two volumes were 101.6 +/- 9.7 and 72.8 +/- 6.8 microliters/100 g, respectively. The kidney weight showed, in contrast a clear increase from 539 to 670 mg/100 g, reflecting the expansion of the proximal and distal tubules due to the increased glomerular filtration rate. It is concluded that although the saline load produced a rise in the renal interstitial pressure, the expected expansion of the interstitium became small, due to the parallel expansion of both the vascular and tubular systems which compress the renal interstitium.

Animals↗
PubMed1984

The influence of tubulo-glomerular feedback on the autoregulation of filtration rate in superficial and deep glomeruli.

Single nephron glomerular filtration rate (SNGFR) of superficial and juxtamedullary nephrons were measured at normal and reduced perfusion pressure in the left kidney of young Sprague Dawley rats. Perfusion pressure was lowered by constricting the aorta proximal to the branching of the left renal artery. The influence of the tubulo-glomerular feedback mechanism on SNGFR was quantitated by measuring SNGFR during intact and interrupted urine flow to the macula densa region. By using a modified Hanssen technique, SNGFR was measured under free-flow conditions. In other experiments, the urine flow to the distal nephron was blocked by a micropuncture technique, which was used for collection of the tubular fluid for measuring the filtration rate. All nephron populations autoregulated SNGFR from 70-80 to 130 mmHg, which was the upper limit of this investigation, when urine flow throughout the nephron was intact. The autoregulation in this pressure range was lost when tubular fluid was prevented from reaching the distal nephron. It was shown that the influence of negative feedback on SNGFR by the macula densa mechanism at normal blood pressure is greater in deep nephrons than in superficial ones.

Animals↗
PubMed1984

The effect of pressor doses of Angiotensin II on autoregulation and intrarenal distribution of glomerular filtration rate in the rat.

This study was designed to investigate the effect of pressor doses of exogenous Angiotensin II (AII) on autoregulation and intrarenal distribution of single nephron glomerular filtration rate (SNGFR) in anesthetized, normotensive rats. SNGFR at all cortical levels of the left kidney was measured with a modified Hanssen technique at three renal arterial pressures (RAP): Spontaneous, 100 +/- 1 mmHg and 70 +/- 1 mmHg. In control rats, both outer cortical (OC) and inner cortical (IC) nephrons showed complete autoregulation of SNGFR when RAP was reduced to 100 +/- 1 mmHg. Further reduction to 70 +/- 1 mmHg resulted in different responses among the cortical layers, accompanying a decrease in SNGFR. The SNGFRIC/SNGFROC ratio increased from 1.36 +/- 0.053 to 1.52 +/- 0.047 and a fractional redistribution of glomerular filtration rate towards IC nephrons was seen. When the kidney was submitted to a RAP of 70 +/- 1 mmHg, there was a concomitant increase in central arterial pressure (CAP) from 120 +/- 4.3 to 134 +/- 3.2 mmHg. A continuous i.v. infusion of AII (0.5 microgram . min-1 . kg-1 BW) increased mean arterial pressure from 123 +/- 1.4 to 142 +/- 3.8 mmHg, an effect corresponding to that on peripheral vascular resistance during reduction of RAP to 70 +/- 1 mmHg in control rats. This dose reduced SNGFR at all cortical levels, but did not per se lead to redistribution of SNGFR. A reduction in RAP to 100 +/- 1 mmHg during AII administration resulted in impaired autoregulation of SNGFR in both OC and IC nephrons.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1982

The tubulo-glomerular feedback mechanism-a determinant for the autoregulation of the glomerular filtration rate in superficial and juxtamedullary nephrons.

The intrinsic myogenic hypothesis and the tubuloglomerular feedback mechanism (TGF) give the presently most cherished explanation to the autoregulation of renal blood flow and glomerular filtration rate. A series of experiments was performed on young, normohydrated rats in order to evaluate the importance of TGF as an autoregulatory factor of the single nephron glomerular filtration rate (SNGFR) in superficial and juxtamedullary nephron populations. Micropuncture techniques were applied to tubular structures of the renal surface and on the papilla for the measurement of hydrostatic pressures and SNGFR. The SNGFR was also measured with a modified Hanssen technique. A TV-technique was used to record the urine free flow rate in the loop of Henle. The net driving forces for glomerular filtration at the afferent end of the glomerular capillaries were estimated to be 19 and 47 mm Hg for superficial and juxtamedullary nephrons respectively, when the urine flow at the macula densa was zero. The SNGFR of the two nephron populations amounted to 29.6 and 84.1 nl . min-1 . g-1 K.W., as measured with the micropuncture technique. With a modified Hanssen technique the corresponding values were 25.8 and 27.7 nl . min-1 . g-1 K.W. (kidney weight). The SNGFR was found to be well autoregulated when the urine flow at the macula densa was intact, but not when the urine flow was interrupted. The flow rate in the loop of Henle was in free flow conditions 7.3 nl . min-1 . g-1 K.W. which shall be compared with 19.2 nl . min-1 . g-1 K.W. when the urine flow to the macula densa was zero. We conclude that SNGFR is mainly autoregulated by the TGF-mechanism in young, normohydrated rats at lower arterial pressures. In normal conditions TGF is highly activated for juxtamedullary nephrons, but not for the superficial ones. The high urine flow rate in the loop of Henle at reduced flow rates at the macula densa may invalidate the use of loop blockade in studies of water and solute transfer across the loop walls.

Animals↗
PubMed1982

Heterogeneity in regulation of glomerular function.

The aim was to study differences in filtration driving forces and glomerular filtration rates between superficial and deep nephrons when urine flow rate was altered at the macula densa region. In young rats stop-flow pressures and single nephron glomerular filtration rates (SNGFR) were measured in the superficial proximal tubules and in the loops of Henle in the papilla. SNGFR was also measured with a modified Hanssen technique. The stop-flow pressures of superficial nephrons amounted to 30.9 +/- 0.8 mmHg (mean +/- SE) and those of juxtamedullary nephrons to 52.2 +/- 1.6 mmHg. In the stop-flow condition the net driving filtration forces were calculated to be about 19 mmHg and 50 mmHg for the superficial and deep glomeruli, respectively. In free flow conditions both net driving forces were calculated to be 19 mmHg. The micropuncture technique gave a SNGFR value for superficial nephrons of 29.6 +/- 2.9 and for deep nephrons of 84.1 +/- 8.5 nl x min-1 . g-1 kidney weight (KW). With a modified Hanssen technique the corresponding values were 25.8 +/- 3.3 and 27.7 +/- 2.9 nl . min-1 . g-1 KW. The tubuloglomerular feedback mechanism is considered to have a powerful regulatory influence on the glomerular filtration rate of deep nephrons.

Animals↗
PubMed1982

Efferent renal nerve activity during intracarotid and intracerebroventricular infusions of hypertonic sodium chloride solutions and isotonic volume expansion in the rat.

The change in renal nerve activity under conditions known to increase renal sodium excretion was studied. In adult Sprague Dawley rats, anaesthetized with Inactin, normotonic and hypertonic NaCl solutions were infused into 1) a vein, 2) a carotid artery and 3) the third ventricle. The left kidney was freed and placed in a plastic cup. A renal nerve was dissected free and placed on a stainless bipolar electrode. The nerve was cut distal to the electrode. The nerve signals were amplified and recorded on a tape recorder. Simultaneously integrated nerve signals and also atrial and venous pressures were recorded. Intracarotid infusion of a 1 M NaCl solution increased sodium output and temporarily decreased renal nerve activity by some 35%. Corresponding intravenous (i.v.) infusion gave an increase in renal nerve activity and also in sodium output. The latter increase was delayed compared with that caused by the intracarotid infusion. No variations in blood pressure were noted. In control experiments with a slow i.v. infusion of physiological saline, renal nerve activity increased throughout the experiment, while sodium excretion remained constant. During infusion of a 1 M NaCl solution into the third ventricle, renal nerve activity decreased in about half of the cases. This reduction was often accompanied by an increased arterial blood pressure and an increased sodium output. Arterial blood pressure increases were especially pronounced at the highest infusion rats, i.e. 800 ml-min-1. Isotonic volume expansion of 2% of the body weight resulted in a transient decrease in renal nerve activity by about 30%. Venous blood pressure rose and sodium output increased six-fold. The decrease in nerve activity was observed both when the vagal nerves were intact and when they were cut.

Animals↗