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PubMed2003

Potassium currents in vestibular type II hair cells activated by hydrostatic pressure.

An elevated hydrostatic pressure in the endolymphatic space of the inner ear is discussed as pathophysiological factor in hydrops-related diseases of the inner ear. An increase in pressure by fractions of 1 cm H(2)O is sufficient to induce vertigo-like symptoms in animal models. To establish a link between hydrostatic pressure and the function of vestibular hair cells, we studied potassium currents in isolated vestibular type II hair cells from guinea-pig utricles when the hydrostatic pressure was increased by raising the height of the bath from 0.2-0.5, 0.7 or 1.0 cm. Elevated pressure enhanced K(+) currents significantly; a rise in pressure from 0.2-0.5 cm H(2)O increased the total K(+) current at +40 mV by 22+/-14% (+/-S.D.). The pressure-sensitive current I(K,p) was non-inactivating during depolarizing pulses. It was maintained when the pressure was kept elevated for several minutes and receded promptly after return to a pressure of 0.2 cm H(2)O. Voltage-gated Ca(2+) currents, in contrast, were not altered by hydrostatic pressure. A pharmacological characterization of I(K,p) revealed that tetraetylammonium (100 mM) abolished all outward currents including I(K,p). I(K,p) was partly and reversibly inhibited by 4-aminopyridine. Dihydrostreptomycin, a blocker of the transduction channel, left I(K,p) unaffected. Charybdotoxin (100 nM), a blocker of Ca(2+)-dependent K(+) channels, completely yet reversibly abolished I(K,p). We conclude that small elevations in hydrostatic pressure evoke a charybdotoxin-sensitive, probably Ca(2+)-dependent K(+) current in vestibular hair cells. This is likely to alter their frequency response and may be a relevant mechanism how hydrostatic pressure disturbs transduction.

Animals↗
PubMed2001

Hydrostatic pressure induced changes in the cytoarchitecture of pheochromocytoma (PC-12) cells.

Confocal microscopy, in association with three-dimensional reconstruction, revealed that microtubules and microfilaments in differentiating PC-12 cells were disrupted in a dose-dependent manner following pressure treatment. Hydrostatic pressure caused cell rounding, microtubule and microfilament disorganization, neurite retraction and the formation of a microtubule ring adjacent to the cell surface. Volume analysis from computer-generated reconstructed cells, at atmospheric pressure, showed that the apparent volume of microtubules and microfilaments, normalized to 100 units, was 22 and 11 respectively. At 4000 and 8000 psi, the apparent microtubule volume was reduced to 16 and 12 units, respectively, and the apparent microfilament volume was reduced to 8 and 5 units, respectively. Thus, the apparent microtubule and microfilament volumes in PC-12 cells decreased as pressure increased. In the presence of taxol and phalloidin which stabilize the cytoarchitecture, cells resist the effects of hydrostatic pressure. In the presence of colchicine and cytochalasin D compounds which destabilize the cytoarchitecture, cells are more susceptible to the disrupting effects of hydrostatic pressure. The effects of hydrostatic pressure on cell morphology were reversible.

Actin Cytoskeleton↗
PubMed1994

Spontaneous changes in arterial blood pressure and renal interstitial hydrostatic pressure in conscious rats.

1. Previous work has demonstrated a positive relationship between experimentally induced changes in arterial pressure (AP) and renal interstitial hydrostatic pressure (RIHP). The purpose of the present study was to test the hypothesis that RIHP is positively correlated with the normal changes in AP that occur spontaneously in conscious rats. 2. Rats were chronically instrumented for the recording of AP (via an aortic catheter) and RIHP. RIHP was measured by implanting a Millar microtransducer, whose tip had been encapsulated in a 35 microns pore polyethylene matrix (5 mm long, 2 mm o.d.), approximately 5 mm below the renal cortical surface. 3. A total of 56 h of simultaneous analog recording of AP and RIHP was obtained from ten rats. Each 1 h segment was digitized and evaluated at frequencies of 1, 0.1, 0.02 and 0.01 Hz. 4. In forty-nine out of fifty-six of these 1 h recordings taken at 1 Hz, there were significant positive linear correlations between AP and RIHP (mean r = 0.32) with a mean slope of 0.11 mmHg RIHP/1 mmHg AP. Low-pass filtering to 0.01 Hz significantly increased the r value to 0.48. 5. These results demonstrate that spontaneous changes in AP and RIHP are positively correlated. The spontaneous coupling of AP and RIHP may be of importance in the regulation of salt and water excretion by the pressure diuresis mechanism.

Anesthesia↗
PubMed1998

Effects of renal perfusion pressure on renal interstitial hydrostatic pressure and Na+ excretion: role of endothelium-derived nitric oxide.

The purpose of this study was to examine the role of endothelium-derived nitric oxide in modulating the effect of renal perfusion pressure (RPP) on renal interstitial hydrostatic pressure (RIHP) and urinary Na+ excretion (UNaV). The effects of RPP on renal hemodynamics, RIHP, and Na+ and Li+ excretions were determined in control Sprague-Dawley rats, in Sprague-Dawley rats pretreated with intravenous infusion of NG-nitro-L-arginine methyl ester (L-NAME) at doses of 1, 5, and 50 microg/kg/min, and in rats pretreated with L-NAME (5 microg/kg/min) plus L-arginine (10 mg/kg/min). The RPP was changed from 95 to 135 mm Hg by an electronically servo-controlled aortic occluder above the renal arteries in all groups. Increasing RPP in control rats from 95 to 135 mm Hg increased RIHP (from 4.4 +/- 0.5 to 8.7 +/- 1.2 mm Hg), UNaV (from 2.37 +/- 0.61 to 8.29 +/- 1.59 microEq/min), and fractional excretion of Li+ (from 38.0 +/- 2.5 to 51.4 +/- 6.0%). In rats pretreated with L-NAME (5 microg/kg/min), increases in RPP from 95 to 135 mm Hg had no effect on RIHP (from 1.6 +/- 0.4 to 2.2 +/- 0.6 mm Hg) or fractional excretion of Li+ and markedly attenuated pressure-natriuresis relationship (from 1.84 +/- 0.50 to 2.88 +/- 0.65 microEq/min). Although L-NAME did reduce renal plasma flow and glomerular filtration rate, the autoregulatory responses to RPP were maintained. In rats pretreated with L-NAME plus L-arginine, RIHP, UNaV, and fractional excretion of Li+ responses to RPP were similar to the control rats. The results of this study indicate that endothelium-derived nitric oxide plays an important role in modulating the effect of RPP on Na+ excretion by enhancing the transmission of RPP into the renal interstitium.

Animals↗
PubMed1995

Effect of renal perfusion pressure on renal interstitial hydrostatic pressure and sodium excretion. Role of vasopressin V1 and V2 receptors.

Renal interstitial hydrostatic pressure (RIHP) has recently been cited as an important mediator of pressure natriuresis. Our objective was to determine the roles of vasopressin V1 and V2 receptors in mediating the effects of renal perfusion pressure (RPP) on RIHP and sodium excretion (UNaV). The effects of RPP on renal hemodynamics, RIHP, and UNaV were assessed in control Wistar rats (n = 10) and in rats pretreated with intravenous infusion of the specific nonpeptide vasopressin V1 antagonist OPC-21268 (100 micrograms.kg-1.min-1; n = 8) and the V2 antagonist OPC-31260 (40 micrograms.kg-1.min-1; n = 10). Increasing RPP from 95 to 118 mm Hg in control rats increased RIHP (6.4 +/- 1.0 to 9.9 +/- 1.3 mm Hg), UNaV (0.29 +/- 0.03 to 0.52 +/- 0.05 muEq.min-1.g-1), urine flow rate (UFR) (5.2 +/- 0.3 to 7.6 +/- 0.6 microL.min-1.g-1), and the fractional excretion of sodium (FENa). In rats pretreated with V1 antagonist, similar results were obtained for urine osmolality and the responses of RIHP, UNaV, UFR, and FENa to RPP. V2 antagonist reduced urine osmolality (392 +/- 47 compared with 979 +/- 88 mOsm.kg-1 in control rats) and enhanced the responses of UNaV (0.43 +/- 0.08 to 1.32 +/- 0.32 microEq.min-1), UFR (17.8 +/- 3.2 to 29.2 +/- 3.8 microL.min-1.g-1), and FENa to RPP, but the RIHP response resembled that observed in the control and V1 antagonist groups. Renal blood flow and glomerular filtration rate did not differ among the three groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2005

Hsp90 inhibitor geldanamycin increases hsp70 mRNA stabilisation but fails to activate HSF1 in cells exposed to hydrostatic pressure.

High hydrostatic pressure (HP) increases Hsp70 protein and mRNA levels by increasing the mRNA half-life without activation of HSF1 transcription factor. We investigated whether this change in gene expression requires Hsp90, previously shown to regulate hsp70 genes via HSF1. In HeLa cells, both HP and Hsp90 inhibitor geldanamycin (GA) up-regulated Hsp70 expression through mRNA stabilisation. GA, unlike HP, increased HSF1 activation. However, when exposures were used together a marked Hsp70 response was observed with mRNA stabilisation without coincidence of HSF1 activation. Our data suggests that Hsp90 is involved in hsp70 mRNA stabilisation and the HSF1 activation can be suppressed by high HP.

Benzoquinones↗
PubMed2006

Fate of Staphylococcus aureus in cheese treated by ultrahigh pressure homogenization and high hydrostatic pressure.

We evaluated the influence of ultrahigh pressure homogenization (UHPH) treatment applied to milk containing Staphylococcus aureus CECT 976 before cheese making, and the benefit of applying a further high hydrostatic pressure (HHP) treatment to cheese. The evolution of Staph. aureus counts during 30 d of storage at 8 degrees C and the formation of staphylococcal enterotoxins were also assessed. Milk containing approximately 7.3 log(10) cfu/mL of Staph. aureus was pressurized using a 2-valve UHPH machine, applying 330 and 30 MPa at the primary and the secondary homogenizing valves, respectively. Milk inlet temperatures (T(in)) of 6 and 20 degrees C were assayed. Milk was used to elaborate soft-curd cheeses (UHPH cheese), some of which were additionally submitted to 10-min HHP treatments of 400 MPa at 20 degrees C (UHPH+HHP cheese). Counts of Staph. aureus were measured on d 1 (24 h after manufacture or immediately after HHP treatment) and after 2, 15, and 30 d of ripening at 8 degrees C. Counts of control cheeses not pressure-treated were approximately 8.5 log(10) cfu/g showing no significant decreases during storage. In cheeses made from UHPH treated milk at T(in) of 6 degrees C, counts of Staph. aureus were 5.0 +/- 0.3 log(10) cfu/g at d 1; they decreased significantly to 2.8 +/- 0.2 log(10) cfu/g on d 15, and were below the detection limit (1 log(10) cfu/g) after 30 d of storage. The use of an additional HHP treatment had a synergistic effect, increasing reductions up to 7.0 +/- 0.3 log(10) cfu/g from d 1. However, for both UHPH and UHPH+HHP cheeses in the 6 degrees C T(in) samples, viable Staph. aureus cells were still recovered. For samples of the 20 degrees C T(in) group, complete inactivation of Staph. aureus was reached after 15 d of storage for both UHPH and UHPH+HHP cheese. Staphylococcal enterotoxins were found in controls but not in UHPH or UHPH+HHP treated samples. This study shows a new approach for significantly improving cheese safety by means of using UHPH or its combination with HHP.

Animals↗
PubMed1992

Hydrostatic pressure mimics gravitational pressure in characean cells.

Hydrostatic pressure applied to one end of a horizontal Chara cell induces a polarity of cytoplasmic streaming, thus mimicking the effect of gravity. A positive hydrostatic pressure induces a more rapid streaming away from the applied pressure and a slower streaming toward the applied pressure. In contrast, a negative pressure induces a more rapid streaming toward and a slower streaming away from the applied pressure. Both the hydrostatic pressure-induced and gravity-induced polarity of cytoplasmic streaming respond identically to cell ligation, UV microbeam irradiation, external Ca2+ concentrations, osmotic pressure, neutral red, TEA Cl-, and the Ca2+ channel blockers nifedipine and LaCl3. In addition, hydrostatic pressure applied to the bottom of a vertically-oriented cell can abolish and even reverse the gravity-induced polarity of cytoplasmic streaming. These data indicate that both gravity and hydrostatic pressure act at the same point of the signal transduction chain leading to the induction of a polarity of cytoplasmic streaming and support the hypothesis that characean cells respond to gravity by sensing a gravity-induced pressure differential between the cell ends.

Calcium↗
PubMed1996

Human red blood cell shape and volume are changed by physiological levels of hydrostatic pressure.

Application of hydrostatic pressure of several atmospheres (atm), such as that applied in diving or hyperbaric treatment, has been previously shown to induce the release of membrane components into the extracellular medium. As the shape of red blood cells (RBC) is sensitive to membrane composition, this might imply a subsequent change in RBC shape and volume. The present study demonstrates that application of hydrostatic pressure of up to 15 atm changes the shape of RBC from the normal discoids to stomatocytes (cup-shaped) and accordingly increases their volume. Changes in RBC shape and volume are known to impair physiological and cellular function. Thus, these changes might be pertinent to hemodynamic and physiological disorders observed in humans subjected to elevated pressure.

Cell Size↗
PubMed1994

[Hydrostatic pressure and neurosurgical pathology].

Hydrostatic pressure is a force applied by a liquid on the surface of an immersed body. Inside the circulatory system it depends on the weight of the blood column between the heart and a given level. In neurosurgical patients, the hydrostatic pressure plays an important role in cerebral perfusion, transcapillary fluid movements and venous air embolism. The mean arterial pressure (Pa), the CSF pressure (CSFP) and the pressure in the jugular vein (JVP) are the hydrostatic determiners of the cerebral perfusion pressure (CPP). The hydrostatic pressure gradient associated with head raising decreases Pa, cerebral venous pressure and JVP, decreases or increases intracranial pressure (ICP) and decreases CPP. The consequences of the resulting hypoperfusion depend on the status of autoregulation. When the skull is open, the pressure under the cerebral retractors determines the transmural pressure and cerebral perfusion. The transcapillary fluid movements depend on a permeability coefficient, a hydrostatic pressure gradient and an osmotic pressure gradient. In case of a rupture of blood brain barrier (BBB), the increase of Pa and the decrease of ICP (craniotomies) favour the development of vasogenic oedema. When the Pa stands higher than the upper limit of autoregulation, the hydrostatic capillary pressure increases. It results in a vasodilation, an increase of cerebral blood flow and oedema, the lesion of BBB being initiated by an increase of the amount and the activity of the pinocytotic vesicles in endothelial cells. The syndrome of BBB rupture at a normal CPP is the consequence of an increase in hydrostatic pressure in the dilated capillary territory and can make more difficult the surgical treatment of arterio-venous malformations.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood-Brain Barrier↗
PubMed1994

Red blood cell aggregability is enhanced by physiological levels of hydrostatic pressure.

The effect of hydrostatic pressure of up to 15 bars on the aggregability of rat and human red blood cells (RBC), i.e., their capability to form aggregates, was studied using computerized image analysis. The aggregate size distribution was determined under ambient pressure, following application of hydrostatic pressure for various durations up to 2 h. It was found that RBC aggregability markedly increases, up to three-fold, as the pressure which had been applied was increased. Accordingly, higher shear stress is required for dispersing the aggregates of pressure-treated RBC than those of untreated cells. The median size of human RBC aggregates was about three times higher than that of rat RBC, and this ratio was maintained following pressure treatment. RBC aggregability is a major determinant in blood flow, especially in the microcirculation. Pressure at the levels used in this study occurs in physiological states such as hyperbaric treatment or diving. The enhanced aggregability induced by application of such pressure implies that blood flow in microvessels might be altered under conditions associated with elevated hydrostatic pressure.

Animals↗
PubMed2001

Do the intervertebral disc cells respond to different levels of hydrostatic pressure?

OBJECTIVE: To test the hypothesis that hydrostatic pressure directly affects the synthesis of collagen and proteoglycan by intervertebral disc cells. DESIGN: By the use of pressure vessels, hydrostatic pressure was applied to intervertebral disc cells cultured in alginate. BACKGROUND: The influence of compression (both hydrostatic and axial) on chondrocyte metabolism was examined in a number of earlier studies. However, in most of these studies, articular cartilage, not intervertebral disc was used, and in none of these was hydrostatic pressure applied to intervertebral disc cells cultured in alginate. METHODS: Fresh cells were harvested from the lumbar intervertebral discs of dogs. Before their suspension in an alginate gel system, the cells were plated and expanded until they reached confluence. Then, by use of the alginate gel system, the cells were exposed (for up to 9 days) to specific values of hydrostatic pressure inside two stainless steel pressure vessels. One vessel was kept at 0.35 MPa and the other at atmospheric pressure (approximately 0.1 MPa). The effects of 0.35 MPa were compared against atmospheric pressure by measuring the incorporation of [3H]-proline and [35S]-sulfate into collagen and proteoglycans, respectively, for the anulus cells and nucleus cells separately, and by determining whether this incorporation was reflected by changes in the levels of mRNA for aggrecan and Types I and II collagen. RESULTS: Proteoglycan synthesis was inhibited at 0.35 MPa as compared to atmospheric pressure for both the nucleus and anulus cells, whereas collagen synthesis was stimulated in the nucleus cells, but inhibited in the anulus cells. The mRNA levels of collagen 1A and collagen 2A decreased in the anulus but showed a differential response in the nucleus (collagen 1A increased, while collagen 2A decreased). The mRNA levels for aggrecan core protein decreased in the anulus and increased in the nucleus. CONCLUSIONS: Hydrostatic pressure directly affects the synthesis of collagen and proteoglycan by the intervertebral disc cells. RELEVANCE: This in vitro study reveals the direct effect of hydrostatic pressure on disc cells, in the absence of other factors. However, circumspection must be applied when comparisons between these results, from in vitro experiments on dog disc cells, are extrapolated and applied to the whole discs of humans.

Alginates↗
PubMed1994

Expression of reduced amounts of structurally altered aggrecan in articular cartilage chondrocytes exposed to high hydrostatic pressure.

The effect of hydrostatic pressure on proteoglycan (PG) metabolism of chondrocyte cultures was examined using a specially designed test chamber. Primary cultures of bovine articular chondrocytes at confluence were exposed for 20 h to 5 and 30 MPa continuous hydrostatic pressures and 5 MPa hydrostatic pulses (0.017, 0.25 and 0.5 Hz) in the presence of [35S]sulphate. Northern blot analyses showed that chondrocyte cultures used in this study expressed abundant mRNA transcripts of aggrecan, typical of chondrocytes, but not versican. The cultures also expressed biglycan and decorin. Enzymic digestions with keratanase and chondroitinases AC, ABC and B and subsequent SDS/agarose gel electrophoresis confirmed the synthesis of aggrecans and small dermatan sulphate PGs. The continuous 30 MPa pressure reduced total PG synthesis by 37% as measured by [35S]sulphate incorporation, in contrast to the 5 MPa continuous pressure which had no effect. The high static pressure also reduced total [3H]glucosamine incorporation by 63% and total [14C]leucine incorporation by 57%. The cyclic pressures showed a frequency-dependent stimulation (0.5 Hz, 11%) or inhibition (0.017 Hz, -17%) of [35S]sulphate incorporation. Aggrecans secreted under continuous 30 MPa pressure showed a retarded migration in 0.75% SDS/agarose gel electrophoresis and they also eluted earlier on Sephacryl S-1000 gel filtration, indicative of a larger molecular size. The increased size was consistent with an increase of average glycosaminoglycan chain length as determined by Sephacryl S-300 gel filtration. No change in aggrecan size was observed with the lower (5 MPa) static or cyclic pressures. Continuous 30 MPa hydrostatic pressure slightly reduced the steady-state mRNA level of aggrecan, in parallel with the decline in PG synthesis measured by [35S]sulphate incorporation. The results demonstrated that high hydrostatic pressure could influence the synthesis of PGs, especially of aggrecans, in chondrocytes both at the transcriptional and translational/post-translational levels.

Aggrecans↗
PubMed1987

Calculated capillary hydrostatic pressure in normal pregnancy and preeclampsia.

Capillary hydrostatic pressure has been calculated in normal pregnancy and preeclampsia. In humans, capillary hydrostatic pressure cannot be measured directly but may be calculated when the colloid osmotic pressure in plasma and interstitial fluid and interstitial fluid hydrostatic pressure are known (Starling equation). New methods have made it possible to measure the interstitial fluid colloid osmotic pressure and interstitial fluid hydrostatic pressure. In the present study interstitial fluid was collected from the subcutaneous tissue by implanted wicks (wick method), and interstitial fluid colloid osmotic pressure was determined. Interstitial fluid hydrostatic pressure was recorded by the wick-in-needle technique. Capillary hydrostatic pressure was calculated in 10 women in the first trimester and 10 in the third trimester of normal pregnancy, in 15 patients with mild preeclampsia, and in 13 women with severe preeclampsia. In normal pregnancy, capillary hydrostatic pressure increased by about 30% between the first and third trimesters. In mild preeclampsia, capillary hydrostatic pressure values did not differ significantly from those in the third trimester of normal pregnancy. However, in severe preeclampsia capillary hydrostatic pressure was significantly lower (40%) than in mild preeclampsia. Whether the low capillary hydrostatic pressure is caused by the severe general vasospasm seen in this condition or is a secondary event is unknown.

Adult↗
PubMed1986

Regulation of sodium excretion by renal interstitial hydrostatic pressure.

Renal interstitial hydrostatic pressure (RIHP) appears to play a crucial role in linking the renal circulation to the rate of tubular reabsorption of sodium and water. Various physiological and pharmacological maneuvers that increase RIHP are associated with increases in sodium excretion. Renal vasodilators that increase RIHP also increase sodium excretion, whereas the vasodilators that do not alter RIHP do not affect sodium excretion. Preventing increases in RIHP during intrarenal infusion of vasodilators markedly attenuates the normal increase in sodium and water excretion. Techniques that directly increase RIHP by renal interstitial volume expansion increase urinary excretion of sodium and water. RIHP may be an important mediator of renal perfusion pressure (RPP) natriuresis. Experimental evidence suggests that the proximal tubule of deep nephrons may be an important nephron site that is sensitive to changes in RPP.

Absorption↗
PubMed1998

Analysis of intracellular pH in the yeast Saccharomyces cerevisiae under elevated hydrostatic pressure: a study in baro- (piezo-) physiology.

Hydrostatic pressure is a distinctive feature of deep-sea environments, and this thermodynamic parameter has potentially inhibitory effects on organisms adapted to living at atmospheric pressure. In the yeast Saccharomyces cerevisiae, hydrostatic pressure causes a delay in or cessation of growth. The vacuole is a large acidic organelle involved in degradation of cellular proteins or storage of ions and various metabolites. Vacuolar pH, as determined using the pH-sensitive fluorescent dye 6-carboxyfluorescein, was analyzed in a hydrostatic chamber with transparent windows under elevated hydrostatic pressure conditions. A pressure of 40-60 MPa transiently reduced the vacuolar pH by approximately 0.33. A vma3 mutant defective in vacuolar acidification showed no reduction of vacuolar pH after application of hydrostatic pressure, indicating that the transient acidification is mediated through the function of vacuolar H(+)-ATPase. The vacuolar acidification was observed only in the presence of fermentable sugars, and never observed in the presence of ethanol, glycerol, or 3-o-methyl-glucose as the carbon source. Analysis of a glycolysis-defective mutant suggested that glycolysis or CO2 production is involved in the pressure-induced acidification. Hydration and ionization of CO2 is facilitated by elevated hydrostatic pressure because a negative volume change (delta V < 0) accompanies the chemical reaction. Moreover the glucose-induced cytoplasmic alkalization is inhibited by elevated hydrostatic pressure, probably because of inhibition of the plasma membrane H(+)-ATPase. Therefore, the cytoplasm tends to become acidic under elevated hydrostatic pressure conditions, and this could be crucial for cell survival. To maintain a favorable cytoplasmic pH, the yeast vacuoles may serve as proton sequestrants under hydrostatic pressure. We are investigating the physiological effects of hydrostatic pressure in the course of research in a new experimental field, baro-(piezo-) physiology.

Environment↗