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C A Tate

Publications and source records attributed to C A Tate.

49 records · Page 3Linked to original sources
PubMed1981

The effect of glucagon on the kinetics of hepatic mitochondrial calcium uptake.

Previous work by this and other laboratories has shown that glucagon administration stimulates calcium uptake by subsequently isolated hepatic mitochondria. This stimulation of hepatic mitochondrial Ca2+ uptake by in vivo administration of glucagon was further characterized in the present report. Maximal stimulation of mitochondrial Ca2+ accumulation was achieved between 6-10 min after the intravenous injection of glucagon into intact rats. Under control conditions, Ca2+ uptake was inhibited by the presence of Mg2+ in the incubation medium. Glucagon treatment, however, appeared to obliterate the observed inhibition by Mg2+ of mitochondrial Ca2+ uptake. Kinetic experiments revealed the usual sigmoidicity associated with initial velocity curves for mitochondrial calcium uptake. Glucagon treatment did not alter this sigmoidal relationship. Glucagon treatment significantly increased the V max for Ca2+ uptake from 292 +/- 22 to 377 +/- 34 nmoles Ca2+/min per mg protein (n = 8) but did not affect the K 0.5, (6.5-8.6 microM). Since the major kinetic change in mitochondrial Ca2+ uptake evoked by glucagon is an increase in V max, the enhancement mechanism is likely to be an increase either in the number of active transport sites available to Ca2+ or in the rate of Ca2+ carrier movement across the mitochondrial membranes.

Animals↗
PubMed1981

Evidence for a calcium-sensitive factor which alters the alkaline pH sensitivity of sarcoplasmic reticulum calcium transport.

Oxalase-supported, ATP-dependent Ca2+ uptake by cardiac and skeletal muscle sarcoplasmic reticulum (SR) exhibits a pH profile with the maximal rate of Ca2+ uptake at pH 6.6-6.8 and marked inhibition (90-95%) at pH 7.4-7.6, a point at which Ca2+-dependent ATPase activity is optimal. These observations are noted when the SR is first preincubated in media containing no added Ca2+. This alkaline pH inhibition is not caused by an irreversible perturbation since the Ca2+ uptake rate is fully restored by changing the alkaline pH preincubation medium to pH 6.8. When SR is preincubated with added Ca2+, Ca2+ uptake at alkaline pH (7.4-7.6) is only inhibited by 10-30%. Ca2+ uptake at pH 6.8 is the same regardless of preincubation conditions. A depressed oxalate permeability is not a factor in the observed alkaline pH inhibition of Ca2+ uptake. At alkaline pH, the relationship between the preincubation Ca2+ concentration and the rate of Ca2+ uptake is hyperbolic; the half-maximal free Ca2+ concentration for stabilization of Ca2+ uptake is 8-15 microM with a Vmax equal to the velocity at the optimal pH. The Hill coefficient is 1.0, implying a single class of Ca2+-requiring sites for stabilization at alkaline pH. In contrast to its effect on Ca2+ uptake, the presence of Ca2+ during preincubation does not alter the pH sensitivity of Ca2+-dependent ATPase activity. Thus, the presence of Ca2+ during preincubation may stabilize a state of the CaATPase, conducive to the coupling of net Ca2+ translocation to Ca2+-dependent ATPase activity, which is ordinarily opposed by alkaline pH. The data suggest a single class of Ca2+-requiring sites which favors this coupled state.

Animals↗
PubMed1980

Calcium uptake by two preparations of mitochondria from heart.

Ca/+ transport and respiratory characteristics of two preparations of cardiac mitochondria (Palmer, J.W., Tandler, B. and Hoppel, C.L. (1977) J. Biol. Chem. 252, 8731-8739) isolated using polytron homogenization (subsarcolemmal mitochondria) and limited Nagarse exposure (intermyofibrillar mitochondria) are described. The Nagarse procedure yields mitochondria with 50% higher rates of oxidative phosphorylation than the polytron-prepared mitochondria in both rat and dog. Rat hear intermyofibrillar mitochondria contain 50% more cytochrome aa3 than the polytron preparation, whereas in the dog, cytochrome aa3 content is not significantly different. Cytochrome oxidase activities and cytochrome c, c1 and b contents were comparable in both populations of rat and dog heart mitochondria. The V of succinate-supported Ca2+ accumulation for Nagarse-prepared mitochondria from rat heart was 1.8-fold higher than the polytron-prepared mitochondria. In dog heart, the Nagarse preparation showed a 3.0-fold higher V for Ca2+ uptake compared to the polytron preparation. A lower apparent affinity for Ca2+ was demonstrated in the intermyofibrillar mitochondria for both species (Km is 2-2.5-fold higher). The Hill coefficient was 1 both mitochondrial types. Subsarcolemmal mitochondria from both species were treated with Nagarse to determine the role of this treatment on the observed differences. Nagarse did not alter any kinetic parameter of Ca2+ uptake. The properties of these mitochondria with reference to their presumed intracellular location may pertain to the role of mitochondria as an intracellular Ca2+ buffering mechanism in contractile tissue.

Absorption↗
PubMed1980

Exercise and mitochondrial calcium transport in the BIO 14.6 hamster.

To examine the effects of exhaustive swimming in normal and myopathic hamsters on muscle mitochondrial Ca2+ metabolism, sedentary normal and BIO 14.6 dystrophic Syrian hamsters swam individually in 35 degree C water until exhaustion occurred. Although the normal hamsters swam three times longer than did the BIO 14.6 hamsters, both swimming groups had a comparable two-fold increase in blood lactate. Contrary to exhaustive running, exhaustive swimming did not significantly affect mitochondrial Ca2+ uptake in either cardiac or skeletal muscle, regardless of the disease state. However, in general, the coefficients of variation for mitochondrial Ca2+ metabolism increased as a function of exercise, with the BIO 14.6 swimmers more variable than the normal swimmers. This suggests that the mitochondrial Ca2+ uptake process may be affected in some manner by exhaustive swimming, so that deviations from the norm are more apparent. The results provide further evidence that mitochondrial Ca2+ metabolism adapts to the specific type of exercise utilized to produce exhaustion.

Adenosine Triphosphate↗
PubMed1980

Populations of rat skeletal muscle mitochondria after exercise and immobilization.

We slightly modified an existing procedure (Palmer et al., J. Biol. Chem. 252: 8731-8739, 1977) to isolate two distinct populations of mitochondria from rat skeletal muscle; initial brief Polytron homogenization released the subsarcolemmal mitochondria, and brief exposure of the resultant intact myofibrils to the proteolytic enzyme, Nagarse, extracted the intermyofibrillar mitochondria. The intermyofibrillar mitochondria differed from the subsarcolemmal mitochondr. ia by higher state III respiration measurements and enzymatic activities. These two populations of mitochondria were then isolated from the gastrocnemius muscle that had been induced to perform different amounts of contractile activity. The endurance training program of daily running significantly increased state III respiration and respiratory control index in the subsarcolemmal mitochondria, but the program did not increase these measurements in the intermyofibrillar mitochondria. In addition, 2 days of hindlimb immobilization resulted in a significant decrease in state II respiration and the respiratory control index of the subsarcolemmal mitochondria; however, immobilization did not affect the intermyofibrillar mitochondria. These measurements suggest that the subsarcolemmal mitochondria adapt in response to chronic changes in the level of contractile activity.

Adaptation, Physiological↗
PubMed1978

Calcium uptake in skeletal muscle mitochondria. I. The effects of chelating agents on the mitochondria from fatigued rats.

Female Wistar rats were used to determine the effects of the chelating agents, EDTA and EGTA, on the in vitro 45Ca2+ accumulation by mitochondria isolated from the skeletal muscle of fatigued animals. The rats were divided into three groups: sedentary-rested (SR), trained-rested (TR), trained-exhausted (TE). The trained groups were exercised on a treadmill for 1 h daily, five times a week, for 22 weeks. At the conclusion of the training program, the TE group was rapidly exercised to exhaustion immediately following their daily 1-h run. In the TR group EDTA reduced 45Ca2+ binding while both EDTA and EGTA appeared to increase mitochondrial Ca2+ and Mg2+ content. In the TE group, EDTA reduced endogenous mitochondrial Ca2+ and Mg2+ content, while both EDTA and EGTA increased 45Ca2+ binding. Since chelating Ca2+ and Mg2+ from the membrane may affect the structure and function of the mitochondria, it is suggested that the use of chelating agents during the isolation of mitochondria from the skeletal muscle of trained rats be viewed with caution.

Animals↗
PubMed1978

Calcium uptake in skeletal muscle mitochondria. II. The effects of long-term chronic and acute exercise.

In order to ascertain the effects of long-term exercise training and long-term exhaustive exercise on mitochondrial 45Ca2+ uptake and related variables in rat skeletal muscle, female rats were randomly divided into three groups: sedentary-rested (SR), trained-rested (TR), and trained-exhausted (TE). The trained groups were exercised five times per week on a treadmill for 22 weeks. At the conclusion of the training period, the TE group was exercised to exhaustion following their daily 1 h run. The 45Ca2+ uptake and endogenous mitochodrial Ca2+ content of skeletal muscle followed stepwise increases of approximately 25% and 50%, respectively, across the groups, suggesting that long-term exercise induces the mitochondria to play an important role as a Ca2+ uptake buffer. A 75--83% reduction in 45Ca2+ binding in the TE group suggests a selective loss and partial saturation of membrane phospholipids with exhaustive exercise. The TE group had a two-fold greater content of mitochondrial Mg2+ than did the rested groups. It is speculated that the mitochondria accumulate Mg2+ during acute exercise to maintain the functional integrity of the membrane, thus offsetting the deleterious effects of excessive Ca2+ uptake

Adaptation, Physiological↗
PubMed1976

Effects of exercise training and exhaustion on 45Ca uptake by rat skeletal muscle mitochondria and sarcoplasmic reticulum.

Mitochondrial and sarcoplasmic reticular 45Ca2+ uptake and Ca2+-ATPase activity were determined in skeletal muscle from exercise trained and non-trained rats at rest or following short-term exhaustive exercise. In trained rats exercised to exhaustion, mitochondrial 45Ca2+ uptake was significantly depressed when compared to non-trained rats at rest. Ca2+-ATPase activity of sarcoplasmic reticulum from trained rats exercised to exhaustion was significantly increased as compared to trained rats at rest. These data suggest that the disruptive influence of Ca2+ accumulation in mitochondria isolated following exhaustive exercise may be diminished as a result of training.

Adenosine Triphosphatases↗
PubMed1975

Changes in erythrocyte 2,3 diphosphoglycerate in women following short term maximal exercise.

15 untrained women were subjected to a walking treadmill test to determine the influence of maximal exercise upon synthesis of erythrocyte 2,3 DPG. Although there was a 9.8% increase in the 2,3 DPG content following exercise, there was a concomitant 9.4% increase in the hemoglobin level; therefore, when 2,3 DPG is expressed as a ratio to hemoglobin (See Article), there was no significant change as a result of exercise stress. It was suggested that three additive factors produced during strenuous exercise; decreased pH; increased hemoglobin concentration; and increased CO2 production result in by-product inhibition of 2,3 DPG synthesis. It is concluded that 2,3 DPG does not provide a physiologic benefit in the adaptation of the oxygen transport system to exercise.

Adult↗
PubMedDate not supplied

Age-related levels of GABA/benzodiazepine binding sites in cerebrum of F-344 rats: effects of exercise.

We examined gamma-aminobutyric acid (GABA), benzodiazepine and convulsant sites of postsynaptic GABA/benzodiazepine receptors (GBZR) in cerebral membranes of inbred Fischer 344 male rats as a function of age. In aged rats (23 to 24 months), the benzodiazepine binding site as determined by [3H]flunitrazepam was 47% and 43% lower than corresponding values in young adult (3 to 4 months) and mature (10 to 12 months) rats, respectively. The decrease was due to the loss of binding density rather than a change in affinity. No statistically significant age-related changes in [3H]muscimol binding were observed when 5 nM or 40 nM labeled muscimol were used. GABA produced a dose-dependent stimulation of flunitrazepam binding in all age groups, but the maximum stimulation in aged animals was significantly higher (24%) than in young and mature animals. The [35S]TBPS binding site, the convulsant site of GABA/benzodiazepine receptors, was unaffected with age. We also studied the effects of exercise on GBZR binding sites of aged rats. The decline of flunitrazepam binding sites and the high sensitivity of flunitrazepam binding to regulation by GABA in aged animals were reversed by 8 to 10 weeks of endurance exercise. Endurance exercise did not have any significant effect on muscimol or TBPS binding sites. Results suggest that there are aged-related alterations of GBZR binding sites and that these modifications can be reversed by exercise.

Aging↗