Heat acclimation and heat stress have different effects on cholinergic-induced calcium mobilization

2001 ◽  
Vol 280 (6) ◽  
pp. R1688-R1696 ◽  
Author(s):  
Pavel Kaspler ◽  
Michal Horowitz
Keyword(s):  
Heat Stress ◽  
Submaxillary Gland ◽  
Heat Acclimation ◽  
Cytosolic Calcium ◽  
Calcium Signal ◽  
Permeabilized Cells ◽  
Fura 2 ◽  
Submaxillary Glands ◽  
Intracellular Ca ◽  
Glandular Cells

There is evidence that the signal transduction array responsible for the secretion of water in evaporative cooling by the submaxillary gland of the rat is subject to heat acclimatory responses. The objectives of the present study were 1) to examine whether heat acclimation affects intracellular Ca2+ mobilization and, in turn, submaxillary glandular responsiveness; 2) to assess whether the acclimatory responses differ from those evoked on heat stress (HS). Experiments were conducted on submaxillary glands of rats acclimated at 34°C for 0, 2 [short-term heat acclimation (STHA)], and 30 [long-term heat acclimation (LTHA)] days. The resting cytosolic calcium concentration ([Ca2+]c) and the carbamylcholine-evoked calcium signal ([Ca2+]s) of dispersed glandular cells were measured using the fluorescent dye fura 2 AM. Inositol-1,4,5-trisphosphate (IP3)-sensitive endoplasmic reticulum Ca2+ stores were determined in permeabilized cells using fura 2 potassium salt. STHA resulted in a drop in both [Ca2+]s and IP3-sensitive Ca2+ stores. On LTHA, the [Ca2+]samplitude reverted to the preacclimation value, whereas the IP3-sensitive Ca2+ stores remained low. The drop in [Ca2+]s on STHA is in accord with the decreased glandular output (measured by 86Rb efflux) observed during this acclimation phase. However, after LTHA the enhanced glandular output despite reduced [Ca2+]s levels suggests an increased efficiency of cellular secretory mechanisms in that group. Collectively, the alterations in [Ca2+]ssupport our biphasic acclimation model (Horowitz M, Kaspler P, Marmari Y, and Oron Y. J Appl Physiol 80: 77–85, 1996.). In nonacclimated glands, HS caused an elevation in [Ca2+]s coincidentally with a decrease in the IP3 Ca2+ stores. In contrast, [Ca2+]s in both STHA and LTHA glands was not affected by HS, despite a marked increase in the IP3-sensitive Ca2+ stores in the LTHA glands. The opposing responses to HS and heat acclimation in calcium signaling and stores confirm the specificity of each process.

scholarly journals The calcium-dependent ATP-Mg/Pi mitochondrial carrier is a target of glucose-induced calcium signalling in Saccharomyces cerevisiae

2005 ◽  
Vol 392 (3) ◽  
pp. 537-544 ◽  
Author(s):  
Santiago Cavero ◽  
Javier Traba ◽  
Araceli Del Arco ◽  
Jorgina Satrústegui
Keyword(s):  
Calcium Binding ◽  
Mitochondrial Protein ◽  
Calcium Signalling ◽  
Cytosolic Calcium ◽  
Calcium Signal ◽  
Transport Activity ◽  
Wild Type ◽  
Binding Motifs ◽  
Mitochondrial Carrier ◽  
Calcium Dependent

Sal1p is a mitochondrial protein that belongs to the SCaMC (short calcium-binding mitochondrial carrier) subfamily of mitochondrial carriers. The presence of calcium-binding motifs facing the extramitochondrial space allows the regulation of the transport activity of these carriers by cytosolic calcium and provides a new mechanism to transduce calcium signals in mitochondria without the requirement of calcium entry in the organelle. We have studied its transport activity, finding that it is a carboxyatractyloside-resistant ATP-Mg carrier. Mitochondria from a disruption mutant of SAL1 have a 50% reduction in the uptake of ATP. We have also found a clear stimulation of ATP-transport activity by calcium, with an S0.5 of approx. 30 μM. Our results also suggest that Sal1p is a target of the glucose-induced calcium signal which is non-essential in wild-type cells, but becomes essential for transport of ATP into mitochondria in yeast lacking ADP/ATP translocases.

Polycythemia and hydration: effects on thermoregulation and blood volume during exercise-heat stress

1988 ◽  
Vol 255 (3) ◽  
pp. R456-R463 ◽  
Author(s):  
M. N. Sawka ◽  
R. R. Gonzalez ◽  
A. J. Young ◽  
S. R. Muza ◽  
K. B. Pandolf ◽  
...  
Keyword(s):  
Heat Stress ◽  
Blood Volume ◽  
Plasma Volume ◽  
Heat Acclimation ◽  
Phosphate Solution ◽  
Stress Tests ◽  
Sweating Rate ◽  
Protein Mass ◽  
Glucose Phosphate ◽  
Humidity Environment

We studied the effects of autologous erythrocyte infusion on thermoregulation and blood volume during exercise in the heat. Specifically, we wanted to determine whether heat-acclimated subjects, as well as hypohydrated subjects, would have a thermoregulatory advantage from acute polycythemia during exercise in the heat. Five heat-acclimated males attempted four heat stress tests (HSTs): two pre- and two postinfusion. Autologous erythrocyte infusion was accomplished with 500 ml of a NaCl-glucose-phosphate solution containing approximately 60% hematocrit. One HST, both pre- and postinfusion, was done while subjects were euhydrated, and one HST was done while subjects were hypohydrated (-5% of body wt). After 30 min of rest in a 20 degrees C antechamber, the HST consisted of a 120-min exposure (2 repeats of 15 min rest and 45 min walking) in a hot (35 degrees C, 45% relative humidity) environment. The findings concerning acute polycythemia in heat-acclimated subjects are summarized: 1) polycythemia increased (P less than 0.05) sweating rate and reduced (P less than 0.01) core temperature during exercise-heat stress for both euhydrated and hypohydrated subjects; 2) the erythrocyte infusion caused an increased (P less than 0.05) plasma volume and increased (P less than 0.01) blood volume; 3) the increased plasma volume was associated with an increased (P less than 0.05) total circulating protein mass; 4) the increased total circulating protein mass tended to better maintain plasma volume when hypohydrated; and 5) heat acclimation may increase extravascular protein mass. Therefore, it is concluded that erythrocyte infusion provides a thermoregulatory advantage during exercise in the heat for heat acclimated subjects when both euhydrated and hypohydrated.

Fura-2 fluorescence is localized to mitochondria in endothelial cells

1987 ◽  
Vol 253 (5) ◽  
pp. C744-C747 ◽  
Author(s):  
S. F. Steinberg ◽  
J. P. Bilezikian ◽  
Q. Al-Awqati
Keyword(s):  
Endothelial Cells ◽  
Calcium Ion ◽  
Cytosolic Calcium ◽  
Ion Concentration ◽  
Homogeneous Distribution ◽  
Aortic Endothelial Cells ◽  
Fura 2 ◽  
Bovine Aortic Endothelial Cells ◽  
Calcium Ion Concentration ◽  
Aortic Endothelial

The new, highly fluorescent, calcium-sensitive dye, fura-2, can be loaded nondisruptively into intact cells by means of its permeant ester and used to measure the free calcium ion concentration in individual cells. For fura-2 to signal cytosolic calcium, it must be distributed homogeneously and exclusively throughout the cytoplasmic space. However, microscopic examination of bovine aortic endothelial cells loaded with fura-2 by exposure to its permeant ester reveals fluorescence associated with discrete intracellular structures rather than the homogeneous distribution expected for a cytosolic stain. Simultaneous labeling of bovine aortic endothelial cells with fura-2 and rhodamine 123 (a mitochondrial fluorescent vital stain) identifies these structures as mitochondria. Subcellular dye localizations are not observed when the cells are loaded with other putative cytosolic stains that gain access to the cytosol by means of a membrane permeant ester. Both carboxyfluorescein and indo-1 (another member of the family of second generation calcium indicators) stain the cytoplasm diffusely. It is suggested that fura-2 fluorescence accumulates in certain cells in association with mitochondria. It is important to assess the intracellular distribution of fura-2 when this indicator is used to measure the free cytosolic calcium ion concentration.

Changes in [Ca2+]i induced by several glucose transport-enhancing stimuli in rat epitrochlearis muscle

2003 ◽  
Vol 94 (5) ◽  
pp. 1813-1820 ◽  
Author(s):  
Shin Terada ◽  
Isao Muraoka ◽  
Izumi Tabata
Keyword(s):  
Glucose Transport ◽  
Quantitative Information ◽  
Dependent Manner ◽  
Sprague Dawley ◽  
Concentration Dependent Manner ◽  
Fura 2 ◽  
Sprague Dawley Rats ◽  
Intracellular Ca ◽  
Resting Muscle ◽  
Krebs Henseleit Buffer

The purpose of the present investigation was to establish a method for estimating intracellular Ca2+ concentrations ([Ca2+]i) in isolated rat epitrochlearis muscles. Epitrochlearis muscles excised from 4-wk-old male Sprague-Dawley rats were loaded with a fluorescent Ca2+indicator, fura 2-AM, for 60–90 min at 35°C in oxygenated Krebs-Henseleit buffer. After fura 2 loading and subsequent 20-min incubation, the intensities of 500-nm fluorescence, induced by 340- and 380-nm excitation lights (Ftotal340 and Ftotal380), were measured. The fluorescences specific to fura-2 (Ffura 2340 and Ffura 2380) were calculated by subtracting the non-fura 2-specific component from Ftotal340 and Ftotal380, respectively. The ratio of Ffura 2340 to Ffura 2380 was calculated as R, and the change in the ratio from the baseline value (ΔR) was used as an index of the change in [Ca2+]i. In resting muscle, ΔR was stable for 60 min. Incubation for 20 min with caffeine (3–10 mM) significantly increased ΔR in a concentration-dependent manner. Incubation with hypoxic Krebs-Henseleit buffer for 10–60 min significantly elevated ΔR, depending on the duration of the incubation. Incubation with 50 μM N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide for 20 min significantly elevated ΔR ( P < 0.05). No significant increases in ΔR were observed during incubation for 20 min with 2 mM 5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside or with 2 mU/ml insulin. These results demonstrated that, by using the fura 2-AM fluorescence method, the changes in [Ca2+]i can be monitored in the rat epitrochlearis muscle and suggest that the method can be utilized to observe quantitative information regarding [Ca2+]i that may be involved in contraction- and hypoxia-stimulated glucose transport activity in skeletal muscle.

scholarly journals FURTHER STUDIES CONCERNING THE FILTRABLE VIRUS PRESENT IN THE SUBMAXILLARY GLANDS OF GUINEA PIGS

1927 ◽  
Vol 46 (6) ◽  
pp. 935-956 ◽  
Author(s):  
Ann G. Kuttner
Keyword(s):  
Guinea Pig ◽  
Guinea Pigs ◽  
Active Material ◽  
Active Agent ◽  
Submaxillary Gland ◽  
Intracerebral Inoculation ◽  
Submaxillary Glands ◽  
Direct Inoculation ◽  
In Series ◽  
Subcutaneous Inoculation

1. It has been shown that the guinea pig virus localizes in the submaxillary glands of young guinea pigs following subcutaneous, intraperitoneal, or intravenous injection of active material, and that the specific lesion is demonstrable in the glands in 12 to 15 days. When an active infection of the gland has been produced in this way, the guinea pigs are refractory to intracerebral inoculation of the virus. 2. No lesion develops in the submaxillary glands of young guinea pigs injected subcutaneously with guinea pig virus which has been inactivated by heat. Young guinea pigs which have received injections of heat-killed virus do not become refractory to intracerebral inoculation of the virus. 3. When young guinea pigs from which both submaxillary glands have been removed are injected subcutaneously with active virus, the virus localizes in the parotid gland, and the animals become refractory to intracerebral inoculation. 4. It has been impossible to demonstrate virucidal properties in the sera of adult guinea pigs which have become spontaneously infected with the virus, or in the sera of young guinea pigs which have been artificially rendered refractory to intracerebral inoculation. 5. It has been possible to transmit the virus from guinea pig to guinea pig continuously in series through seven animals by direct inoculation from submaxillary gland to submaxillary gland. 6. The fact that the virus regularly localizes in the submaxillary glands following subcutaneous inoculation has been utilized in passing the virus from guinea pig to guinea pig. 2 weeks after the subcutaneous inoculation of the virus into young guinea pigs, the active agent was present in the submaxillary glands. Emulsions of the submaxillary glands of these animals were then used for the subcutaneous injection of another group of young guinea pigs. In this way the virus was transmitted continuously from skin to submaxillary gland through a series of seven animals.

Heat acclimation, aerobic fitness, and hydration effects on tolerance during uncompensable heat stress

1998 ◽  
Vol 84 (5) ◽  
pp. 1731-1739 ◽  
Author(s):  
Stephen S. Cheung ◽  
Tom M. McLellan
Keyword(s):  
Heart Rate ◽  
Heat Stress ◽  
Aerobic Fitness ◽  
Protective Clothing ◽  
Sweat Rate ◽  
Heat Acclimation ◽  
Short Term ◽  
Chemical Protective Clothing ◽  
Uncompensable Heat Stress ◽  
C 30

—The purpose of the present study was to determine the separate and combined effects of aerobic fitness, short-term heat acclimation, and hypohydration on tolerance during light exercise while wearing nuclear, biological, and chemical protective clothing in the heat (40°C, 30% relative humidity). Men who were moderately fit [(MF); <50 ml ⋅ kg−1 ⋅ min−1maximal O2 consumption; n = 7] and highly fit [(HF); >55 ml ⋅ kg−1 ⋅ min−1maximal O2 consumption; n = 8] were tested while they were euhydrated or hypohydrated by ∼2.5% of body mass through exercise and fluid restriction the day preceding the trials. Tests were conducted before and after 2 wk of daily heat acclimation (1-h treadmill exercise at 40°C, 30% relative humidity, while wearing the nuclear, biological, and chemical protective clothing). Heat acclimation increased sweat rate and decreased skin temperature and rectal temperature (Tre) in HF subjects but had no effect on tolerance time (TT). MF subjects increased sweat rate but did not alter heart rate, Tre, or TT. In both MF and HF groups, hypohydration significantly increased Tre and heart rate and decreased the respiratory exchange ratio and the TT regardless of acclimation state. Overall, the rate of rise of skin temperature was less, while ΔTre, the rate of rise of Tre, and the TT were greater in HF than in MF subjects. It was concluded that exercise-heat tolerance in this uncompensable heat-stress environment is not influenced by short-term heat acclimation but is significantly improved by long-term aerobic fitness.

Force relaxes before the fall of cytosolic calcium in the photomechanical response of rat sphincter pupillae

2000 ◽  
Vol 279 (1) ◽  
pp. C274-C280 ◽  
Author(s):  
Andrew P. Krivoshik ◽  
Lloyd Barr
Keyword(s):  
Myosin Light Chain ◽  
Smooth Muscles ◽  
Cytosolic Calcium ◽  
Myosin Phosphorylation ◽  
Primary Signal ◽  
Intracellular Ca ◽  
Phosphorylation Cascade ◽  
Muscle Myosin ◽  
Light Flashes ◽  
Stimulation Of

In the rat sphincter pupillae, as in other smooth muscles, the primary signal transduction cascade for agonist activation is receptor → G protein → phospholipase C → inositol trisphosphate → intracellular Ca2+concentration ([Ca2+]i) → calmodulin → myosin light chain kinase → phosphorylated myosin → force development. Light stimulation of isolated sphincters pupillae can be very precisely controlled, and precise reproducible photomechanical responses (PMRs) result. This precision makes the PMR ideal for testing models of regulation of smooth muscle myosin phosphorylation. We measured force and [Ca2+]iconcurrently in sphincter pupillae following stimulation by light flashes of varying duration and intensity. We sampled at unusually short (0.01–0.02 s) intervals to adequately test a PMR model based on the myosin phosphorylation cascade. We found, surprisingly, contrary to the behavior of intestinal muscle and predictions of the phosphorylation model, that during PMRs force begins to decay while [Ca2+]iis still rising. We conclude that control of contraction in the sphincter pupillae probably involves an inhibitory process as well as activation by [Ca2+]i.

scholarly journals QUANTITATIVE STUDIES OF PROSTATIC SECRETION

1953 ◽  
Vol 97 (5) ◽  
pp. 663-680 ◽  
Author(s):  
Charles Huggins ◽  
John Lambert Sommer
Keyword(s):  
Structural Changes ◽  
Testosterone Propionate ◽  
Estrogenic Activity ◽  
Submaxillary Gland ◽  
Critical Factors ◽  
Simple Arithmetic ◽  
Estrogenic Compounds ◽  
Submaxillary Glands ◽  
Quantitative Studies ◽  
Prostatic Epithelium

The prostate of the dog was relocated permanently in the perineum where its size could be measured and correlated with the output of prostatic secretion during many months. The secretion of a submaxillary gland obtained through a fistula was utilized as an internal biologic standard of the effects of pilocarpine, the secretory stimulus employed, because the amount and route of administration of the alkaloid are critical factors in inducing secretion. Prostatic secretion was found to be profoundly affected by androgenic and estrogenic compounds, in contrast to salivation. The curves of the secretory response of the prostate and submaxillary glands to pilocarpine proved to be similar and a mathematical formula has been constructed to represent them. When testosterone propionate was administered in increasing quantities for periods of weeks at each level, the volume of the prostate increased in a series of flattened curves. This volume, under the conditions mentioned, was found to stand in a simple arithmetic relationship to the amount of testosterone propionate administered. Moderate quantities of testosterone propionate masked the effects of small amounts of stilbestrol on the prostate. The reverse was also true and the critical amounts of these compounds were defined. The amounts of stilbestrol were determined which lowered the quantity of prostatic secretion resulting from the simultaneous administration of moderate amounts of testosterone propionate in castrate dogs, the result being a level and flat secretory curve which was maintained for many weeks. We designate this effect the plateau phenomenon. When this amount of estrogen was continued, and the dosage of testosterone propionate greatly augmented, the prostatic secretion did not increase in volume. Very slight increases above the critical amount of stilbestrol, however, caused the secretory curve to fall to new and still lower levels though the secretion was never completely suppressed. The acid phosphatase content of the prostatic secretion in the regions of secretory plateaus was similar to that of castrate dogs injected with androgen alone. The plateau phenomenon is due to simultaneous physiologic action of androgenic and estrogenic compounds on the prostatic cells. The depression of prostatic secretion resulting in the plateau phenomenon is due to both functional and structural changes in the prostatic epithelium. They are best explained on the assumption that differences in steroid threshold exist in groups of cells within the prostate, those of the anterior rim of the gland being least susceptible to estrogenic activity.

scholarly journals GH gene expression in the submaxillary gland in normal and Ames dwarf mice

2001 ◽  
Vol 169 (2) ◽  
pp. 389-396 ◽  
Author(s):  
A Perez-Romero ◽  
E Dialynas ◽  
F Salame ◽  
A Amores ◽  
L Vidarte ◽  
...  
Keyword(s):  
Southern Blot ◽  
Submaxillary Gland ◽  
Rt Pcr ◽  
Submaxillary Glands ◽  
Ames Dwarf Mice ◽  
Igf I ◽  
Ames Dwarf ◽  
Heart Blood ◽  
Two Parameters ◽  
Dwarf Mice

High local GH-releasing hormone (GHRH) levels are capable of inducing transdifferentiation in salivary cells to synthesize GH. However, the factors implicated in this process remain unknown. To study this subject, normal and Ames dwarf mice were implanted in the submaxillary gland with a slow release pellet releasing 21 microgram GHRH (1-29)-NH(2)/day for 2 months. Control animals received placebo pellets at the same site. After 60 days, heart blood was collected and submaxillary glands were removed. Circulating levels of GH and IGF-I were significantly decreased (P<0.05) in dwarf mice in comparison with controls, and GHRH treatment did not modify either of these two parameters. Controls carrying GHRH pellets showed a significantly higher GH content (P<0.05) in the submaxillary gland than the placebo-treated normal mice. There were no differences between the IGF-I concentrations of placebo- and GHRH-treated salivary tissue from normal mice. Analysis of GH mRNA by RT-PCR followed by Southern blot revealed that GH transcripts were present in the salivary gland samples carrying the placebo pellets in both normal and dwarf mice. The expression of GH was significantly (P<0.05) increased by the GHRH pellets in salivary tissue from normal mice, but not in submaxillary glands from dwarf mice. Pit-1 mRNA was not detected in the GHRH-treated glands of normal and dwarf mice by RT-PCR or by Southern blot. Using these highly sensitive methods, we have been able to detect the transcription of both GH and Pit-1 in pituitaries from Pit-1-deficient Ames dwarf mice. The present experiment demonstrates that salivary tissue synthesizes GH when it is exposed to the influence of GHRH. Both basal and GHRH-induced salivary GH expression appear to be independent of Pit-1.

Analysis of elongating morphogenesis of quail anterior submaxillary gland: absence of localized cell proliferation

Development ◽  
1981 ◽  
Vol 62 (1) ◽  
pp. 229-239
Author(s):  
Hiroyuki Nogawa
Keyword(s):  
Cell Proliferation ◽  
Basement Membrane ◽  
Regional Differences ◽  
Submaxillary Gland ◽  
Mesenchymal Cells ◽  
Submaxillary Glands ◽  
Parallel Direction ◽  
Recombination Experiments

Quail anterior submaxillary glands elongated extensively without branching (more than sevenfold) from 8 to 10 incubation days. Investigation of mitotic activity of the rudiments in vivo showed no localized cell proliferation throughout the rudiments, and recombination experiments in vitro to examine regional differences in mitogenic activity of the surrounding mesenchyme also showed that no mesenchymal region specifically stimulates the epithelial cell proliferation. Histological observation of the rudiments showed that epithelial cells did not lengthen in a parallel direction to the long axis of the rudiment, and that mesenchymal cells encircled the epithelial cord perpendicularly to its axis. The basement membrane was obscure in the distal end of the rudiments, while it was easily detected in the other part of the rudiments. These results suggest that the elongating morphogenesis of the anterior submaxillary rudiments is not achieved by localized cell proliferation but by almost uniformly distributed cell proliferation, and mesenchymal cells surrounding the rudiment or the basement membrane may be involved in the controlling mechanisms of the elongating morphogenesis.

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