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M Salomonsson

Publications and source records attributed to M Salomonsson.

14 recordsLinked to original sources
PubMed1992

Lack of effect of intraluminal pressure on renin release from isolated afferent arterioles.

To evaluate the role of the proposed baroreceptor mechanism in the afferent arteriole in regulating renin release, we modified the isolated perfused tubule technique to perfuse afferent arterioles. Arterioles with attached glomeruli were isolated from rabbit kidneys and perfused using standard methods. To stop the arteriolar flow and allow perfusion pressure, as set by a mercury manometer, to be built up in the lumen of the vessel, the glomerulus was sucked into a constriction pipette. The preparation was continuously superfused with Krebs-Ringer solution in the first series of experiment, and a cell culture medium in the second series of experiment. The superfusate droplets were collected under mineral oil with 10-min collection intervals. The renin content of the samples was assayed by radioimmunoassay of the angiotensin I generated. In the two series of experiments we tested the effects of sequential changes in intraluminal pressure on renin release. In the first series of experiments (n = 6) the renin release was 56.3 nGU arteriole-1 min-1 in the first 10 min of sampling. The renin release was then constant for 80 min with an average of 21.6 nGU arteriole-1 min-1. In the last 30 min the renin release was 96.5 nGU arteriole-1 min-1. In the second series of experiments (n = 8) the renin release was 26.5 nGU arteriole-1 min-1 throughout the course of the experiment. These results indicate that under these conditions there is no relation between renin release and intraluminal pressure in afferent arterioles.

Animals↗
PubMed1991

Intracellular cytosolic free calcium concentration in the macula densa and in ascending limb cells at different luminal concentrations of sodium chloride and with added furosemide.

The juxtaglomerular apparatus fulfils several important regulatory functions in the kidney, such as tubuloglomerular feedback (TGF) control and control of renin release. The macula densa (MD) cells sense the fluid load by perceiving the distal NaCl concentration via a Na-K-2Cl cotransport system in the luminal cell membrane. It has been proposed that macula densa cell activation may involve changes in intracellular cytosolic free calcium concentration ([Ca2+]i), as one link in the chain of events activating TGF or releasing renin. We therefore investigated the changes in the intracellular calcium concentrations with fura-2, using a video system, in macula densa cells, and compared them with the changes in the corresponding concentrations in the ascending limb of the loop of Henle (c-TAL). The results show that our technique for analysing intracellular cytosolic free calcium in isolated perfused tubules is valid for this purpose, and the Kd value obtained was similar to that found by Grynkiewicz et al. (1985). The intracellular cytosolic free calcium concentration was about 90 nM both in the macula densa and c-TAL cells, and the macula densa cell intracellular cytosolic free calcium concentration increased by about 20 nM when the tubular lumen was perfused with Na and Cl at low concentrations. No significant changes were noted when furosemide was added to the perfusion solutions. We consider it hardly likely that this small change in intracellular cytosolic free calcium concentration can be entirely responsible for full activation of renin release or full inactivation of the TGF control mechanism. It would seem that the signal transmission from the macula densa cells could occur by other routes than through activation of intracellular cytosolic free calcium concentration.

Animals↗
PubMed1991

Mechanisms of renin release from juxtaglomerular cells.

In microdissected, nonperfused afferent arterioles changes in intravascular pressure did not affect renin secretion. On the contrary, renin release from isolated afferent arterioles perfused in a free-flow system has been reported to be sensitive to simultaneous changes in luminal pressure and flow. Hence local blood flow may be involved in the baroreceptor control of renin release. If flow is sensed, the sensor is likely to be located near the endothelial cell layer, where ion channels have been shown to be influenced by variations in shear stress.

Animals↗
PubMed1991

Macula densa cell function.

Studies concerning the sensing step in the tubuloglomerular feedback (TGF) mechanism have been conflicting. To study this step, we measured macula densa (MD) cell volume and membrane potentials in the isolated perfused ascending limb of the loop of Henle with attached glomerulus with MD segments (cTAL-MD). Addition of furosemide reduced cell volume rapidly and the effect could be reversed on removal of the drug. From the time course of cell volume changes hydraulic conductivity could be measured both in the basolateral and apical cell membrane. It was found that the apical cell membrane constituted the main barrier for water flow with a low hydraulic conductance, while the basolateral hydraulic conductance was quite high. Measurements of the basolateral electrical potential in the MD cells have shown a mean electrical potential of -56 mV. This potential was hyperpolarized by the addition of furosemide, the Cl channel blocker NPPB, or during a reduction of luminal NaCl from 150 to 30 mM, and depolarized when bath Cl concentration was reduced from 150 to 30 mM. These results are consistent with the following model for electrolytes transported and similar to the one described in the cTAL [15]. In the luminal cell membrane there is an Na-K-2Cl cotransporter that takes these ions into the MD cells and there is a potassium recycling through a K channel. On the basolateral membrane side there is an Na-K pump and a Cl channel through which chloride is transported out of the MD cell. The Na-K pump activity seems to be only 1/40 of that in the cTAL cells.(ABSTRACT TRUNCATED AT 250 WORDS)

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PubMed1991

Chloride concentration in macula densa and cortical thick ascending limb cells.

The Cl- transport through the macula densa (MD) cells is believed to be a link in the tubuloglomerular feedback (TGF) believed to be a link in the tubuloglomerular feedback (TGF) mechanism and MD-mediated renin release. One step in this transport is probably the electroneutral and furosemide-sensitive Na(+)-K(+)-2Cl- contransport on the luminal membrane of MD cells. Another step is transport through basolateral Cl- channels. In the present study the intracellular Cl- concentration, [Cl-]i, was measured in the MD and cortical thick ascending limb (cTAL) cells, and the concentration changes elicited by blocking the Na(+)-K(+)-2Cl- cotransport with furosemide or by lowering the luminal NaCl concentration determined. We also investigated the effects of blocking the basolateral Cl- channels. A preparation consisting of a segment of the cTAL, MD cells, and the attached glomerulus was dissected from rabbit kidneys. The preparation was loaded with the Cl(-)-sensitive fluorophore SPQ, and perfused by using the isolated and perfused tubule technique. The intracellular chloride concentration was determined with a video system using digital imaging that measured the intensity of the emitted SPQ fluorescence. The T 1/2 of the leakage of SPQ was found to be (197 +/- 60) min (n = 9). With 150 mM NaCl in the lumen and bath, [Cl-]i in MD cells was 47 +/- 13 mM (n = 8) and 54 +/- 13 mM (n = 5) in cTAL cells. When furosemide (10(-4) M) was added to the luminal perfusion, the MD cell [Cl-]i was reduced to 6 +/- 2 mM. The corresponding value in cTAL cells was 5 +/- 3 mM.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Optical studies on the action of furosemide on macula densa and cortical thick ascending limb cells. Intracellular calcium fluorescence measurements.

The present study shows the successful use of an optical technique that describes the application of both differential interference contrast (DIC) and fluorescence microscopy to the study of structure-function relationships in isolated perfused cTAL-MD segments of the nephron. Image-intensified video microscopy and digital image processing techniques were used to simultaneously and directly visualize and quantify [Ca+2]i in individual cTAL cells and MD cells. This study also indicates that no large changes in MD [Ca+2]i can be observed under maneuvers that are known to affect the autoregulatory mechanisms of single nephron glomerular filtration rate. Therefore, it is less likely that MD [Ca+2]i could be a link in the transmission of the signal from the MD cells to the rest of the cells in the juxtaglomerular apparatus for the release of the TGF mechanism and/or renin. Possibly some other mechanism like the electrolyte transport itself, that can alter the solute concentration and tonicity of the Goormaghtigh cell field (juxtaglomerular interstitium), may be the signal to proceed with the rest of the events developed by the juxtaglomerular apparatus to control single nephron glomerular filtration rate.

Animals↗
PubMed1989

Macula densa cells sense luminal NaCl concentration via furosemide sensitive Na+2Cl-K+ cotransport.

The macula densa cells of the juxtaglomerular apparatus probably serve as the sensor cells for the signal which leads to the appropriate tubuloglomerular feedback response. The present study reports basolateral membrane voltage (PDbl) measurements in macula densa cells. We isolated and perfused in vitro thick ascending limb segments with the glomerulus, and therefore the macula densa cells, and the early distal tubule still attached. Macula densa cells were impaled with microelectrodes under visual control. PDbl was recorded in order to examine how these cells sense changes in luminal NaCl concentrations. The addition of furosemide, a specific inhibitor of the Na+2Cl-K+ cotransporter in the thick ascending limb, to the lumen of the perfused thick ascending limb hyperpolarized PDbl from -55 +/- 5 mV to -79 +/- 4 mV (n = 7). Reduction of NaCl in the lumen perfusate from 150 mmol/l to 30 mmol/l also hyperpolarized PDbl from -48 +/- 3 mV to -66 +/- 5 mV (n = 4). A Cl- concentration step in the bath from 150 mmol/l to 30 mmol/l resulted in a 24 +/- 4 mV (n = 4) depolarization of PDbl. This depolarization of PDbl was absent when furosemide was present during the Cl- concentration step. These data suggest that the macula densa cells sense changes in luminal NaCl concentration via coupled uptake of Na+ and Cl-.(ABSTRACT TRUNCATED AT 250 WORDS)

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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.

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