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A Chinet

Publications and source records attributed to A Chinet.

11 recordsLinked to original sources
PubMed1992

Ca(2+)-dependent heat production under basal and near-basal conditions in the mouse soleus muscle.

1. The rate of energy expended for the clearance of sarcoplasmic Ca2+ by sarcoreticular Ca2+ uptake process(es), plus the concomitant metabolic reactions, was evaluated from measurements of resting heat production by mouse soleus muscle before and after indirect inhibition of Ca2+ uptake by sarcoplasmic reticulum (SR). 2. Direct inhibition of the Ca2+, Mg(2+)-ATPase of SR membrane in intact muscle preparations exposed to the specific inhibitor 2,5-di(tert-butyl-1,4-benzohydroquinone (tBuBHQ) slowly increased the rate of heat production (E). Indirect inhibition of SR Ca2+ uptake was obtained by reducing sarcoplasmic Ca2+ concentration (Ca2+i) as a consequence of reducing Ca2+ release from the SR using dantrolene sodium. This promptly decreased E by 12%. Exposure of the preparations to an Mg(2+)-enriched environment (high Mg2+) or to the chemical phosphatase 2,3-butanedione monoxime (BDM), two other procedures aimed at decreasing SR Ca2+ release, also acutely decreased E, by 20 and 24%, respectively. 3. Subthreshold-for-contracture depolarization of the sarcolemma achieved by increasing extracellular K+ concentration to 11.8 mM induced a biphasic increase of E: an initial peak to 290% of basal E, followed by a plateau phase at 140% of basal E during which resting muscle tension was increased by less than 3%. Most, if not all, of the plateau-phase metabolic response was quickly suppressed by dantrolene or high Mg2+ or BDM. Another means of increasing SR Ca2+ cycling was to partially remove the calmodulin-dependent control of SR Ca2+ release using the calmodulin inhibitor W-7. The progressive increase in E with 30 microM-W-7 was largely reduced by dantrolene or high Mg2+ or BDM. 4. In the presence of either dantrolene or BDM to prevent the effect of W-7 on SR Ca2+ release, exposure of the muscle to W-7 acutely suppressed about 3% of E. This and the above results confirm that the plasmalemmal, calmodulin-dependent Ca(2+)-ATPase, although a qualitatively essential part of the Ca2+i homeostatic system of the cell, can only be responsible for a very minor part of the energy expenditure devoted to the homeostasis of Ca2+i. Active Ca2+ uptake by SR which, at least in the submicromolar range of Ca2+i, is expected to be responsible for most of this Ca(2+)-dependent energy expenditure, might dissipate up to 25-40% of total metabolic energy in the intact mouse soleus under basal and near-basal conditions.

Animals↗
PubMed1990

Control of respiration in skeletal muscle at rest.

The suggestion is made that, under resting conditions in situ, muscle cell respiration is dependent on the way O2 and substrates are distributed to the cells by the microcirculation. (Delivery is measured as arterial-blood concentration multiplied by flow to the organ.) Microscale heterogeneity of this distribution, which is more marked but less stable than the more easily demonstrated larger-scale heterogeneity (0.1 to 0.5-g sampling grain), might indeed ration O2 and substrates in a large population of the cells of a resting organ at any given moment, and microscale heterogeneity of distribution may thus take part in the normal control of cell respiration.

Animals↗
PubMed1989

Evidence by calorimetry for an activation of sodium-hydrogen exchange of young rat skeletal muscle in hypertonic media.

1. The rate of energy dissipation associated with Na(+)-H+ exchange in isolated, superfused soleus muscles from young rats was measured with an isothermal microcalorimeter during quasi-stationary states of oxidative metabolism. 2. Under normal physiological conditions, amiloride, an inhibitor of the Na(+)-H+ exchange across plasma membranes, had no measurable effect on the specific rate of muscle heat production (E); the ouabain-suppressible part of E was identical whether amiloride was absent or present. 3. E was increased under hyperosmotic conditions and the difference with respect to control (excess E) was proportional to the degree of hyperosmolarity of the superfusate. It was 48% of basal E during a +100 mosM stress (with no change of extracellular Na+ concentration, Na+o). Inhibition of Ca2+ release into the sarcoplasm with sodium dantrolene (10(-5) M) or tetracaine (5 x 10(-5) M) suppressed a substantial part (65 and 53%, respectively) of the steady-state excess E (1.2 mW (g wet weight)-1) induced by the +100 mosM stress. Practically 100% of excess E was suppressed in the nominal absence of extracellular sodium (Na+o = 0, Li+ substitution) or under 15 mM-Na+o, and excess E was enhanced when Na+o was increased (hyperosomolarity by addition of Na2SO4 instead of sucrose). 4. Under hyperosmotic conditions, amiloride at the 5 x 10(-7) M concentration had no effect on excess E whereas at 10(-4) M it induced a significant decrease of excess E. The absolute effect of 10(-4) M-amiloride was -0.34 mW (g wet weight)-1 (equal to 28% of the excess E due to a +100 mosM-sucrose stress and to 14% of the excess E due to a +100 mosM-Na2SO4 stress). It was left unaltered in the presence of dantrolene and was independent of the way the +100 mosM stress was obtained (i.e. 100 mM-sucrose or 50 mM-Na2SO4). It was suppressed at Na+o = 0-15 mM and could be mimicked by guanochlor, another potent inhibitor of Na(+)-H+ exchange. In the presence of 10(-4) M-amiloride, the ouabain-suppressible E was significantly reduced. In the presence of ouabain, amiloride had no effect. 5. Muscle tissue space available to [3H]inulin was measured in parallel experiments. It was 23.3% under control conditions and 30.6% after a 2 h exposure of the muscle to a +100 mosM-Na2SO4 stress.(ABSTRACT TRUNCATED AT 400 WORDS)

Amiloride↗
PubMed1985

Brown adipose tissue heat production in heat acclimated and perchlorate treated rats.

The noradrenaline-induced energy dissipation rate was measured with a direct microcalorimeter in brown adipose tissue taken from rats acclimated to 34 degrees C (HA), perchlorate treated (PC) and heat acclimated-perchlorate treated (HAPC). The response to 10(-7) M NA was reduced by 45%, 47% and 86% in HA, PC and HAPC groups, respectively, as compared to a control group kept at 24 degrees C. In the same groups, the response to 10(-6) M NA was reduced by 34%, 7% and 64%, respectively. The specific activity of the soluble alpha-glycerophosphate dehydrogenase in brown fat from HA rats was reduced by 50%, whereas it was not altered in the PC animals. It is concluded that the sensitivity to noradrenaline of the brown adipose tissue thermogenic mechanisms is decreased in hypothyroidism, and that the acclimation temperature and the thyroid status per se each have a different influence on brown adipose tissue function.

Acclimatization↗
PubMed1979

Pulmonary O2 diffusing capacity estimates from assumed log-normal VA/Q distributions.

Steady-state pulmonary gas exchange has been measured in hypoxia in 33 mongrel dogs with the aim of comparing DLO2 estimates obtained with three procedures differing by the models assumed for functional inhomogeneity. In the first procedure the lung was assumed to be homogeneous and the corresponding DLO2 estimate was 15 mumol . min-1. Torr-1 . kg-1. In the second procedure, which is the one commonly used in respiratory physiology, alveolar dead space was considered as the unique form of functional inhomogeneity and the corresponding DLO2 estimate was 31 mumol . min-1. Torr-1 . kg-1. In the third procedure, which has been specially worked out for this study, functional inhomogeneity was represented by a log-normal distribution of the VA/Q ratios and the corresponding DLO2 estimate was 50 mumol . min-1 . Torr-1 . kg-1. The relation between the DLO2 estimates by the second and by the third procedures was found to depend upon the blood pH. This could be explained on the basis of the effects of acidosis on the blood capacitances for O2 and for CO2. Analysis suggests that in hypoxia where normally the O2 capacitance is about half the CO2 one, the third procedure yields DLO2 estimates about twice as large as those obtained by the second one.

Animals↗
PubMed1979

Thyroid hormones and the energetics of active sodium-potassium transport in mammalian skeletal muscles.

1. The steady-state heat production rate (E) of soleus muscles obtained from adult mice in various thyroid states was measured in a perfused microcalorimeter. The ouabain-suppressible fractions of E and 42K influx were compared and the energetic efficiency of active Na-K transport assessed. 2. Hypothyroidism with plasma thyroxine concentrations below 1 microgram/100 ml. was induced by pretreatment with 131I or perchlorate. In soleus muscles isolated from treated animals, mean E values were 25.1 +/- 0.7 and 24.2 +/- 0.5 mcal.g wet wt.-1.min-1 for the 131I and the perchlorate series respectively, i.e. about 30% lower than the control level (36.3 +/- 1.5 mcal.g wet wt.-1.min-1). Following triiodothyronine treatment, E was increased by about 45%. 3. In muscles from hypothyroid (131I and perchlorate series), euthyroid and hyperthyroid mice ouabain (10(-3) M) induced a rapid decrease in E of 1.6 +/- 0.1 and 1.4 +/- 0.1, 2.5 +/- 0.2, and 4.3 +/- 0.6 mcal.g wet wt.-1.min-1 respectively, i.e. between 6 and 8% of E. 4. In muscles obtained from hypothyroid, euthyroid and hyperthyroid mice, the ouabain-suppressible component of 42K influx was 0.17 +/- 0.04, 0.31 +/- 0.02 and 0.45 +/- 0.02 micromole. g wet wt.-1.min-1 respectively. Whereas the total number of ouabain binding sites varied appreciably with the thyroid status, the Na-K contents of soleus or diaphragm muscles showed no significant changes. 5. Notwithstanding the parallelism between the changes in basal E and ouabain-sensitive components of E and K influx with the thyroid status, it is concluded that active NA-K transport cannot be considered a primary effector of thyroid thermogenesis in intact mammalian skeletal muscle. The direct contribution of active NA-K transport to this thermogenesis was indeed small compared with the over-all cellular energy dissipation. 6. The minimum over-all energetic efficiency of the transport process in the intact muscles (30--35%) was not dependent on the thyroid status.

Animals↗
PubMed1978

Does cytoplasmic alkalinization trigger mitochondrial energy dissipation in the brown adipocyte?

Indirect calorimetry measurements showed that brown fat thermogenesis was very sensitive to modifications of intra-cellular pH induced by extracellular acid-base perturbations. Specific blockage of active Na-K transport by ouabain inhibited the thermogenic response only in acidosis and more efficiently when the glycoside was administered before the catecholamine stimulus than when it was added after the full calorigenic response had developed. It is suggested that the catecholamine stimulus might initiate a positive feed-back alkalinization of the cytoplasm, concomitant with activation of Na-K transport.

Adipose Tissue, Brown↗
PubMed1978

Comparative measurements of in vitro thermogenesis of brown adipose tissue from control and cold adapted rats.

Heat output and oxygen uptake rates as well as caloric equivalents of O2 were measured in brown fat fragments from cold-adapted and control rats. Resting metabolic rate per unit wet weight was the same in both groups. Submaximal responses to noradrenaline were significantly lower in the cold-adapted than in the control group. Apparent maximal responses were the same for both groups. Caloric equivalents of O2 gave no evidence for anaerobic glycolysis even under conditions of oxygen limitation.

Acclimatization↗
PubMed1977

Microcalorimetric determination of energy expenditure due to active sodium-potassium transport in the soleus muscle and brown adipose tissue of the rat.

1. The resting heat production rate (E) of soleus muscles from young rats and brown adipose tissue from adult rats was measured by means of a perfusable heat flux microcalorimeter in the absence and presence of ouabain. In the soleus muscle, the acute response of E to ouabain was compared with the ouabain-suppressible components of 22Na-efflux and 42K-influx. 2. In standard Krebs-Ringer bicarbonate buffer, ouabain (10(-3)M) induced an immediate but transient decrease in E of around 5%. Both in muscle and adipose tissue this was followed by a progressive rise in heat production rate. 3. When the medium was enriched with Mg (10 mM), ouabain produced a sustained decrease in E of the same magnitude as in the standard medium and the secondary rise was less marked or abolished. Under these conditions, in the soleus muscle, ouabain inhibited E by 5% (i.e. by 1-76 +/- 0-22 mcal.g wet wt.-1.min-1), 22Na-efflux by 58% (0-187 +/- 0-013 micronmole. g wet wt.-1.min-1) and 42K-influx by 34% (0-132 +/- 0-028 micronmole. g wet wt.-1.min-1). 4. When the muscles were loaded with Na by pre-incubation in K-free Mg-enriched medium, the addition of K (3mM) induced an immediate ouabain-suppressible increase in E of 2-98 +/- 0-33 mcal. g wet wt.-1.min-1 and a concomitant stimulation of 22Na-efflux of 0-388 +/- 0-136 micronmole. g wet wt.-1.min-1. 5. Maximum Na/ATP ratios for the active Na-K transport process were computed, with no assumption as to the in vivo free energy of ATP hydrolysis. These were 2-1, 1-9 and 2-3 under the conditions described in paragraphs (2), (3) and (4) respectively. 6. The calculated reversible thermodynamic work associated with active Na-K transport corresponded to 34% of the measured ouabain-induced decrease in E. On the premise that the maximum efficiency of the cellular energy conservation processes is 65%, this estimate indicates that the minimum energetic efficiency of ATP utilization by the active Na-K transport process in mammalian muscle is 52%.

Adenosine Triphosphate↗
PubMed1975

Potassium-induced increase in oxygen consumption of brown adipose tissue from the rat.

1. In brown adipose tissue, noradrenaline induces an increase in respiration and a depolarization of the cells. The effect of an increase in potassium concentration in a range known to depolarize the brown adipocytes was tested on the O2 consumption. 2. Isolated interscapular brown adipose tissue from the rat was incubated in chambers that allowed O2 consumption to be measured over prolonged periods. 3. 45-50 mM-KC1 were found to induce a more that fourfold increase in O2 consumption, which was stable, reversible and dependent upon the presence of calcium in the meduim. 4. When rats were pre-treated with reserpine or 6-hydroxydopamine the KC1-induced increase in O2 consumption was sharply reduced or entirely adsent. 5. The effect of KC1 was greatly inhibited by (-)-propranolol, but not by (+)-propranolol. 6. Moderate increases in O2 consumption induced by low concentrations of potassium were potentiated by desipramine, a drug which is known to block the uptake of catecholamines by adrenergic nerve endings. 7. Surgical denervation caused a decrease in the catecholamine content of the tissue, but had no effect on the KC1 response. 8. It is concluded that in brown adipose tissue, potassium stimulates O2 consumption by causing a release of noradrenaline from nerve endings. This implies that surgical denervation as it is commonly performed on this tissue does not denervate the brown adipocytes but probably only the blood vessels.

Adipose Tissue, Brown↗