Relationship between motility and oxygen consumption of sperm from the cauda epididymides of the rat

1999 ◽  
Vol 11 (2) ◽  
pp. 87 ◽  
Author(s):  
R. N. Murdoch ◽  
R. C. Jones ◽  
V. L. Armstrong ◽  
J. Clulow
Keyword(s):  
Oxygen Consumption ◽  
Respiration Rate ◽  
Sperm Motility ◽  
Dibutyryl Camp ◽  
Epididymal Sperm ◽  
Exogenous Substrate ◽  
Individual Effects ◽  
Rate Of Oxygen Consumption ◽  
Stimulation Of

The oxygen consumption of rat sperm was low (2.7 µL O2 108 sperm–1h–1) in caudal epidi-dymal semen (CES) when stimulation of motility was avoided. The addition of 1 µL of Krebs Ringer phosphate buffer (KRP) to 40 µL of CES (CES : KRP = 40 : 1) did not activate motility, but stimulated oxygen consumption 2-fold. Inclusion of 1–5 mМ glucose, acetate, pyruvate or lactate in the KRP further stimulated respiration rate (up to 4.3-fold) without activating motility, but respiration was reduced when 2- deoxyglucose replaced energy substrates. Inclusion of dibutyryl cAMP (1 mM) activated sperm motility in all samples and stimulated oxygen consumption 2.9-fold. Dilution of CES at the ratio of CES : KRP = 40 : 1000 also activated sperm motility and stimulated respiration rate 2.9-fold. The combined effect of dibutyryl cAMP and glucose in stimulating respiration was greater than their individual effects. However, the response to cAMP or substrates was not altered by incubation in KRP containing either 0 or 0.5 mM Ca2+. It was concluded that the motility and metabolism of rat epididymal sperm are suppressed in vivo. Respiration can be stimulated by a small (1.025-fold) dilution and further stimulated by the inclusion of energy substrate, without activating motility. However, a larger dilution or inclusion of cAMP activated motility and simultaneously stimulated metabolism, with exogenous substrate being required to stimulate respiration to the maximum rate. This suggests that prior to activation, the rate of oxygen consumption and sperm motility are not coupled.

scholarly journals Role of cAMP/PKA signaling cascade in vasopressin-induced trafficking of TRPC3 channels in principal cells of the collecting duct

2010 ◽  
Vol 298 (4) ◽  
pp. F988-F996 ◽  
Author(s):  
Monu Goel ◽  
Cheng-Di Zuo ◽  
William P. Schilling
Keyword(s):  
Apical Membrane ◽  
Collecting Duct ◽  
Surface Membrane ◽  
Transient Receptor Potential Channels ◽  
Signaling Cascade ◽  
Dibutyryl Camp ◽  
Principal Cells ◽  
V2 Receptor ◽  
Stimulation Of

Transient receptor potential channels TRPC3 and TRPC6 are expressed in principal cells of the collecting duct (CD) along with the water channel aquaporin-2 (AQP2) both in vivo and in the cultured mouse CD cell line IMCD-3. The channels are primarily localized to intracellular vesicles, but upon stimulation with the antidiuretic hormone arginine vasopressin (AVP), TRPC3 and AQP2 translocate to the apical membrane. In the present study, the effect of various activators and inhibitors of the adenylyl cyclase (AC)/cAMP/PKA signaling cascade on channel trafficking was examined using immunohistochemical techniques and by biotinylation of surface membrane proteins. Both in vivo in rat kidney and in IMCD-3 cells, translocation of AQP2 and TRPC3 (but not TRPC6) was stimulated by [deamino-Cys1, d-Arg8]-vasopressin (dDAVP), a specific V2-receptor agonist, and blocked by [adamantaneacetyl1, O-Et-d-Tyr2, Val4, aminobutyryl6, Arg8,9]-vasopressin (AEAVP), a specific V2-receptor antagonist. In IMCD-3 cells, translocation of TRPC3 and AQP2 was activated by forskolin, a direct activator of AC, or by dibutyryl-cAMP, a membrane-permeable cAMP analog. AVP-, dDAVP-, and forskolin-induced translocation in IMCD-3 cells was blocked by SQ22536 and H89, specific inhibitors of AC and PKA, respectively. Translocation stimulated by dibutyryl-cAMP was unaffected by AEAVP but could be blocked by H89. AVP- and forskolin-induced translocation of TRPC3 in IMCD-3 cells was also blocked by two additional inhibitors of PKA, specifically Rp-cAMPS and the myristoylated inhibitor of PKA (m-PKI). Quantification of TRPC3 membrane insertion in IMCD-3 cells under each assay condition using a surface membrane biotinylation assay, confirmed the translocation results observed by immunofluorescence. Importantly, AVP-induced translocation of TRPC3 as estimated by biotinylation was blocked on average 95.2 ± 1.0% by H89, Rp-cAMPS, or m-PKI. Taken together, these results demonstrate that AVP stimulation of V2 receptors in principal cells of the CD causes translocation of TRPC3 to the apical membrane via stimulation of the AC/cAMP/PKA signaling cascade.

scholarly journals Brief Vibrotactile Stimulation Does Not Increase Cortical Oxygen Consumption When Measured by Single Inhalation of Positron Emitting Oxygen

1999 ◽  
Vol 19 (3) ◽  
pp. 260-265 ◽  
Author(s):  
Shinsuke Ohta ◽  
David C. Reutens ◽  
Albert Gjedde
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Sensory Cortex ◽  
Vibrotactile Stimulation ◽  
Step Method ◽  
Brain Oxygen ◽  
One Step ◽  
The One ◽  
Stimulation Of

Vibrotactile stimulation of the hand elicits no increase in oxygen consumption commensurate with the increase in blood flow measured in human sensory cortex. To test the hypothesis that previous failures to detect a proportionate increase in oxygen consumption could be an artefact of the sequential bolus, or three-step, method used to measure this parameter in the human brain in vivo, the authors compared the measurements with the results of a novel single bolus, or one-step, method of measuring oxygen consumption. The time of completion of the three-step method was 40 to 50 minutes, whereas the one-step method lasted only 3 minutes. The baseline whole-brain oxygen consumption averaged 185 ± 32 μmol hg−1 min−1 by the three-step method and 153 ± 15 μmol hg−1 min−1 by the one-step method. Vibrotactile stimulation did not elicit a significant increase in oxygen consumption measured by either method. This finding rejects the hypothesis that failure to detect an increase of oxygen consumption could be an artefact caused by limitations of the method used previously. Conversely, it also rejects the hypothesis that observations of an increase of oxygen consumption by the new method are artefacts caused by limitations of the one-step method.

scholarly journals Stimulation of Oxygen Consumption with Fluid Absorption in Insect Recta

1982 ◽  
Vol 101 (1) ◽  
pp. 233-254
Author(s):  
D.F. HOULIHAN ◽  
D. SELL
Keyword(s):  
Oxygen Consumption ◽  
Time Course ◽  
Fluid Injection ◽  
Fluid Absorption ◽  
Fluid Uptake ◽  
Local Osmosis ◽  
Before And After ◽  
Rate Of Oxygen Consumption ◽  
Stimulation Of

The oxygen consumption of excised abdomens of cockroaches and locusts has been measured before and after the injection of fluids into the ligated recta. Fluid injection caused a transient stimulation of oxygen consumption of up to 30% of the resting rate. The extra amount of oxygen consumed is positively correlated with the osmolality of the fluid injected and the amount of fluid absorbed. Parallel experiments were carried out on the time course of fluid uptake; these experiments revealed a correlation first between a rapid increase in fluid absorption and stimulation of oxygen consumption, and secondly between the final resting rate of oxygen consumption and a slower absorption of fluid. Locusts take up fluid at double the rate of cockroaches and have double the stimulation in oxygen consumption following fluid injection. In locusts the increases in oxygen consumption can also be correlated with the net movement of Na+, K+and Cl− from the rectum. The stimulation of oxygen consumption during fluid uptake is discussed in relation to the local osmosis model for fluid uptake.

scholarly journals Glycolysis in Neurons, Not Astrocytes, Delays Oxidative Metabolism of Human Visual Cortex during Sustained Checkerboard Stimulation in vivo

2001 ◽  
Vol 21 (12) ◽  
pp. 1384-1392 ◽  
Author(s):  
Albert Gjedde ◽  
Sean Marrett
Keyword(s):  
Oxygen Consumption ◽  
Visual Cortex ◽  
Glucose Metabolism ◽  
Oxidative Metabolism ◽  
Time Course ◽  
Complex Stimulus ◽  
Neuronal Activation ◽  
Positron Emission ◽  
Stimulation Of

The regulation of brain energy metabolism during neuronal activation is poorly understood. Specifically, the extent to which oxidative metabolism rather than glycolysis supplies the additional ATP necessary to sustain neuronal activation is in doubt. A recent hypothesis claims that astrocytes generate lactate with the muscle-type lactate dehydrogenase (LDH) isozyme LD5. Lactate from astrocytes then undergoes oxidation in neurons after reconversion to pyruvate by the LDH subtype LD1. On the basis of this hypothesis, the authors predicted that the time course of an excitatory increase of the oxidative metabolism of brain tissue must depend on the degree to which astrocytes provide neurons with pyruvate in the form of lactate. From the known properties of the LDH subtypes, the authors predicted two time courses for the changes of oxygen consumption in response to neuronal stimulation: one reflecting the properties of the neuronal LDH subtype LD1, and the other reflecting the astrocytic LDH subtype LD5. Measuring oxygen consumption (CMR o2) with positron emission tomography, the authors demonstrated increased CMR o2 during sustained stimulation of visual cortex with a complex stimulus. The CMR o2 increased 20.5% after 3 minutes and 27.5% after 8 minutes of stimulation, consistent with a steady-state oxygen–glucose metabolism ratio of 5.3, which is closest to the index predicted for the LD1 subtype. The index is equal to the oxygen–glucose metabolism ratio of 5.5 calculated at baseline, indicating that pyruvate is converted to lactate in a cellular compartment with an LDH reaction closest to that of LD1, whether at rest or during stimulation of the visual cortex with the current stimulus. The findings are consistent with a claim that neurons increase their oxidative metabolism in parallel with an increase of pyruvate, the latter generated by neuronal rather than astrocytic glycolysis.

scholarly journals THE INSENSITIVITY OF PARAMECIUM TO CYANIDE AND EFFECTS OF IRON ON RESPIRATION

1931 ◽  
Vol 15 (1) ◽  
pp. 107-118 ◽  
Author(s):  
Charles S. Shoup ◽  
James T. Boykin
Keyword(s):  
Oxygen Consumption ◽  
Respiration Rate ◽  
Iron Content ◽  
Paramecium Caudatum ◽  
Ph Values ◽  
Iron Salts ◽  
Stimulation Of

1. The effects of KCN and iron salts on oxygen consumption has been studied in the cell of Paramecium caudatum by manometric methods. 2. KCN solutions of strengths from M/200 to M/10,000 have been shown to produce no decrease in oxygen consumption, but have in most cases produced a very slight increase in the respiration rate. 3. The pH values were found to have little or no effect on these results. 4. Iron salts produce either no effect or a great diminution of oxygen consumption, in no case causing stimulation of rates of respiration. 5. Iron salts in neutral solutions do not penetrate the Paramecium cell nor do they cause so marked an effect as in an acid state. 6. The iron-content of Paramecium was found to be extremely small and not demonstrable by delicate tests. It is believed that iron is not combined in the cell in the form of a respiration-catalyst sensitive to cyanide.

Lack of interaction between acid and pepsinogen secretion in isolated gastric glands

1983 ◽  
Vol 245 (6) ◽  
pp. G775-G779
Author(s):  
S. J. Hersey ◽  
M. Miller ◽  
D. May ◽  
S. H. Norris
Keyword(s):  
Cyclic Nucleotides ◽  
Acid Formation ◽  
Dibutyryl Camp ◽  
Gastric Glands ◽  
Isolated Gastric Glands ◽  
Pepsinogen Secretion ◽  
Inhibited Acid ◽  
Weak Stimulation ◽  
Stimulation Of

Gastric glands isolated from rabbit stomach were employed to study the relation between acid and pepsinogen secretion. The effects of adenosine and guanosine nucleotides were examined for both secretory processes. cAMP, dibutyryl cAMP (DBcAMP), and 8-bromo-cAMP (8BrcAMP) were found to stimulate both acid and pepsinogen secretion with a potency sequence of 8BrcAMP greater than DBcAMP greater than cAMP. Adenosine, ATP, and AMP were ineffective, indicating that the responses to adenosine cyclic nucleotides do not involve an adenosine receptor. 8BrcGMP was found to produce a weak stimulation of both acid and pepsinogen secretions, while GMP, cGMP, and DBcGMP were ineffective. DBcGMP was found to inhibit competitively the stimulation of pepsinogen secretion by cholecystokinin (CCK)-like peptides. No inhibition was found with cGMP or 8BrcGMP. Stimulation of pepsinogen secretion by carbachol or isoproterenol was not inhibited by DBcGMP nor was the stimulation of acid formation by CCK-like peptides. Thiocyanate inhibited acid formation but did not affect pepsinogen secretion stimulated by 8BrcAMP or carbachol, indicating that stimulation of pepsinogen secretion does not require simultaneous acid formation. Costimulation of acid formation by histamine and pepsinogen secretion by isoproterenol showed no interaction between the two secretory processes. The results are interpreted to suggest that correlations between acid and pepsinogen secretion observed in vivo do not result from direct interactions between parietal and chief cells.

RELATIONSHIP OF RESPIRATION RATE TO TEMPERATURE IN A SUPERCOOLED INSECT

1958 ◽  
Vol 36 (3) ◽  
pp. 265-268 ◽  
Author(s):  
R. W. Salt
Keyword(s):  
Oxygen Consumption ◽  
Respiration Rate ◽  
Cold Hardiness ◽  
Heat Injury ◽  
Rate Of Oxygen Consumption ◽  
Cold Hardy ◽  
Logarithmic Relationship ◽  
Relationship Of

The rate of oxygen consumption of mature larvae of Anagasta kühniella (Zell.) exhibits a logarithmic relationship to temperature over a range extending from the limit of supercooling to the beginning of heat injury. This information supplements that of Scholander et al. (4), who demonstrated the same relationship in frozen Chironomus larvae, the rate being lower than in supercooled forms and hence not continuous with the above-zero portion of the curve. Together, these two simple relationships invalidate Kozhantschikov's theory of cold-hardiness based on a thermostable respiration below 0 °C. in cold-hardy insects and no respiration in frozen non-cold-hardy insects.

THE ROLE OF LACTATE IN THE STIMULATION OF THE OXYGEN CONSUMPTION OF FROG MUSCLE BY INSULIN

1964 ◽  
Vol 42 (1) ◽  
pp. 139-151 ◽  
Author(s):  
D. R. H. Gourley ◽  
Kenneth C. Fisher
Keyword(s):  
Oxygen Consumption ◽  
Major Effect ◽  
Ringer Solution ◽  
Frog Muscle ◽  
Complete Oxidation ◽  
Rate Of Oxygen Consumption ◽  
Lactate Utilization ◽  
Stimulation Of ◽  
Extra Oxygen

Lactate, citrate, succinate, or acetate added to isolated muscles suspended in Ringer solution in a Warburg flask produced an increase in the rate of oxygen consumption by the muscles. At a given molar concentration of these substances the increase was greatest with lactate and was progressively less with the addenda in the order given. When the concentration of each substance was adjusted so that the rate of oxygen consumption was the same with all of them, the addition of insulin produced an increase in the oxygen uptake which was of the same magnitude in each case. Evidence is presented which suggests that by causing spontaneous activity in the muscle, the acetate, succinate, and citrate may bring about a production of lactate.The extra oxygen consumed upon the addition of lactate could account for the complete oxidation of only a small part of the lactate which actually disappeared in an experiment. By assuming that all of this extra oxygen was used in the complete oxidation of lactate, it was calculated from the total lactate utilization in the presence or absence of insulin that the major effect of insulin was on the fraction of utilized lactate which was oxidized. This conclusion was also suggested by experiments with monoiodoacetate.

scholarly journals Non-signalling energy use in the developing rat brain

2016 ◽  
Vol 37 (3) ◽  
pp. 951-966 ◽  
Author(s):  
Elisabeth Engl ◽  
Renaud Jolivet ◽  
Catherine N Hall ◽  
David Attwell
Keyword(s):  
Oxygen Consumption ◽  
Information Processing ◽  
Rat Brain ◽  
Energy Use ◽  
Brain Slices ◽  
Lipid Synthesis ◽  
Processing Power ◽  
Mature Brain ◽  
Rate Of Oxygen Consumption

Energy use in the brain constrains its information processing power, but only about half the brain's energy consumption is directly related to information processing. Evidence for which non-signalling processes consume the rest of the brain's energy has been scarce. For the first time, we investigated the energy use of the brain's main non-signalling tasks with a single method. After blocking each non-signalling process, we measured oxygen level changes in juvenile rat brain slices with an oxygen-sensing microelectrode and calculated changes in oxygen consumption throughout the slice using a modified diffusion equation. We found that the turnover of the actin and microtubule cytoskeleton, followed by lipid synthesis, are significant energy drains, contributing 25%, 22% and 18%, respectively, to the rate of oxygen consumption. In contrast, protein synthesis is energetically inexpensive. We assess how these estimates of energy expenditure relate to brain energy use in vivo, and how they might differ in the mature brain.

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